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opa1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc opa1
    COPN restores mitochondrial quality control and interrupts the ROS‒cGAS‒inflammation axis in OGD/R-treated R28 cells. a , TEM images showing changes in the mitochondrial ultrastructure of R28 cells subjected to various treatments (PBS, PDNs, COPN-L, and COPN-H) after OGD/R. Scale bar: 500 nm b , Quantitative analyses of mitochondrial length and number in R28 cells as indicated in a . c , Representative fluorescence images showing JC-1 staining of the mitochondrial Δψm: aggregates (red) indicate healthy mitochondria, whereas monomers (green) represent depolarized mitochondria. Nuclei were stained with DAPI (blue). Scale bar: 50 μm d , Intracellular ATP content assay revealing improved energy production after COPN treatment under OGD/R stress conditions. e , mRNA expression analysis of mitochondrial dynamic regulatory genes <t>(Opa1,</t> Mfn2, Drp1, and Fis1) and mitochondrial DNA transcription levels (mt-ND1 and mt-COX1). f , Quantitative analysis of the JC-1 fluorescence ratio (aggregates/monomers) and mitochondrial ROS levels (MitoSOX staining). g–h , Western blot analysis of proteins involved in mitochondrial autophagy (Pink1, Parkin, and P62) (g) and mitochondrial fusion/fission (Opa1, Mfn2, Mfn1, Drp1, and Fis1) (h) . i , Confocal fluorescence microscopy images of mitochondria (green, MitoTracker) and lysosomes (red, LysoTracker) in R28 cells after different treatments. Nuclei were stained with Hoechst (blue). Scale bar: 50 μm ∗ ∗∗∗P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
    Opa1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 412 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+opa1+antibody/OPA1+Rabbit+mAb/pmc13049686-160-30-31
    Average 96 stars, based on 412 article reviews
    opa1 - by Bioz Stars, 2026-10
    96/100 stars

    Images

    1) Product Images from "A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation"

    Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

    Journal: Materials Today Bio

    doi: 10.1016/j.mtbio.2026.102974

    COPN restores mitochondrial quality control and interrupts the ROS‒cGAS‒inflammation axis in OGD/R-treated R28 cells. a , TEM images showing changes in the mitochondrial ultrastructure of R28 cells subjected to various treatments (PBS, PDNs, COPN-L, and COPN-H) after OGD/R. Scale bar: 500 nm b , Quantitative analyses of mitochondrial length and number in R28 cells as indicated in a . c , Representative fluorescence images showing JC-1 staining of the mitochondrial Δψm: aggregates (red) indicate healthy mitochondria, whereas monomers (green) represent depolarized mitochondria. Nuclei were stained with DAPI (blue). Scale bar: 50 μm d , Intracellular ATP content assay revealing improved energy production after COPN treatment under OGD/R stress conditions. e , mRNA expression analysis of mitochondrial dynamic regulatory genes (Opa1, Mfn2, Drp1, and Fis1) and mitochondrial DNA transcription levels (mt-ND1 and mt-COX1). f , Quantitative analysis of the JC-1 fluorescence ratio (aggregates/monomers) and mitochondrial ROS levels (MitoSOX staining). g–h , Western blot analysis of proteins involved in mitochondrial autophagy (Pink1, Parkin, and P62) (g) and mitochondrial fusion/fission (Opa1, Mfn2, Mfn1, Drp1, and Fis1) (h) . i , Confocal fluorescence microscopy images of mitochondria (green, MitoTracker) and lysosomes (red, LysoTracker) in R28 cells after different treatments. Nuclei were stained with Hoechst (blue). Scale bar: 50 μm ∗ ∗∗∗P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
    Figure Legend Snippet: COPN restores mitochondrial quality control and interrupts the ROS‒cGAS‒inflammation axis in OGD/R-treated R28 cells. a , TEM images showing changes in the mitochondrial ultrastructure of R28 cells subjected to various treatments (PBS, PDNs, COPN-L, and COPN-H) after OGD/R. Scale bar: 500 nm b , Quantitative analyses of mitochondrial length and number in R28 cells as indicated in a . c , Representative fluorescence images showing JC-1 staining of the mitochondrial Δψm: aggregates (red) indicate healthy mitochondria, whereas monomers (green) represent depolarized mitochondria. Nuclei were stained with DAPI (blue). Scale bar: 50 μm d , Intracellular ATP content assay revealing improved energy production after COPN treatment under OGD/R stress conditions. e , mRNA expression analysis of mitochondrial dynamic regulatory genes (Opa1, Mfn2, Drp1, and Fis1) and mitochondrial DNA transcription levels (mt-ND1 and mt-COX1). f , Quantitative analysis of the JC-1 fluorescence ratio (aggregates/monomers) and mitochondrial ROS levels (MitoSOX staining). g–h , Western blot analysis of proteins involved in mitochondrial autophagy (Pink1, Parkin, and P62) (g) and mitochondrial fusion/fission (Opa1, Mfn2, Mfn1, Drp1, and Fis1) (h) . i , Confocal fluorescence microscopy images of mitochondria (green, MitoTracker) and lysosomes (red, LysoTracker) in R28 cells after different treatments. Nuclei were stained with Hoechst (blue). Scale bar: 50 μm ∗ ∗∗∗P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Techniques Used: Control, Fluorescence, Staining, Expressing, Western Blot, Microscopy

    Related Articles

    Expressing:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Standard Deviation:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Control:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Western Blot:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Negative Control:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Isolation:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Activity Assay:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Marker:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    High Molecular Weight:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.

    Immunoprecipitation:

    Article Title: Mitochondrial elongation confers protection against doxorubicin-induced cardiotoxicity.
    Article Snippet: Doxorubicin (DOX)-induced cardiac damage remains a leading cause of death amongst cancer survivors.. DOXinduced cardiotoxicity (DIC) is mediated by disturbed mitochondrial dynamics, but it remains debated that the mechanisms by which DOX disrupted equilibrium between mitochondrial fission and fusion.. In the present study, we observed that DOX induced mitochondrial elongation in multiple cardiovascular cell lines.

    Article Title: RVG29 and platelet membrane-modified pseudo-mitochondria for cascade targeting of cyclosporin a in traumatic brain injury.
    Article Snippet: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide.. Cyclosporin A (CsA) is a promising drug for TBI, as it can protect neuronal mitochondria from dysfunction and apoptosis.. However, CsA also has serious limitations, such as poor blood-brain barrier (BBB) penetration, non-selective distribution characteristic, and immunosuppressive effects.

    Article Title: A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury
    Article Snippet: Anti-OPA1 antibody , Cell Signaling Technology , Cat#80471; RRID:AB_2734117.



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    96
    Cell Signaling Technology Inc opa1
    COPN restores mitochondrial quality control and interrupts the ROS‒cGAS‒inflammation axis in OGD/R-treated R28 cells. a , TEM images showing changes in the mitochondrial ultrastructure of R28 cells subjected to various treatments (PBS, PDNs, COPN-L, and COPN-H) after OGD/R. Scale bar: 500 nm b , Quantitative analyses of mitochondrial length and number in R28 cells as indicated in a . c , Representative fluorescence images showing JC-1 staining of the mitochondrial Δψm: aggregates (red) indicate healthy mitochondria, whereas monomers (green) represent depolarized mitochondria. Nuclei were stained with DAPI (blue). Scale bar: 50 μm d , Intracellular ATP content assay revealing improved energy production after COPN treatment under OGD/R stress conditions. e , mRNA expression analysis of mitochondrial dynamic regulatory genes <t>(Opa1,</t> Mfn2, Drp1, and Fis1) and mitochondrial DNA transcription levels (mt-ND1 and mt-COX1). f , Quantitative analysis of the JC-1 fluorescence ratio (aggregates/monomers) and mitochondrial ROS levels (MitoSOX staining). g–h , Western blot analysis of proteins involved in mitochondrial autophagy (Pink1, Parkin, and P62) (g) and mitochondrial fusion/fission (Opa1, Mfn2, Mfn1, Drp1, and Fis1) (h) . i , Confocal fluorescence microscopy images of mitochondria (green, MitoTracker) and lysosomes (red, LysoTracker) in R28 cells after different treatments. Nuclei were stained with Hoechst (blue). Scale bar: 50 μm ∗ ∗∗∗P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
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    Image Search Results


    Rhy enhances mitochondrial function by promoting mitochondrial fusion. (A) Representative fluorescent images of mitochondria stained with Mito-tracker Red in PC12 cells. (B) Quantitative analysis of mitochondrial networks in PC12 cells using the MiNA plugin for ImageJ ( n = 5 images). (C) Mitochondrial morphology in primary midbrain neurons visualized by Mito-tracker Red. (D) Mitochondrial network parameters quantified by MiNA analysis in primary midbrain neurons ( n = 5 images). (E) High-resolution imaging of mitochondrial inner membranes using PKmito Orange (PKMO) microscopy. (F) Representative transmission electron microscopy (TEM) images of mitochondrial ultrastructure. (G) Mitochondrial membrane potential quantification by JC-1 ratio (Red/Green) in PC12 cells and primary midbrain neurons, n = 3 independent experiments. (H) Cellular ATP levels determined using ATPlite™ luminescence assay ( n = 3). (I) Western blotting analysis of DRP1, p-DRP1 Ser616 , p-DRP1 Ser637 , MFN2 and OPA1 levels, following 6-OHDA (150 μmol/L) and Rhy treatment (1, 2, 5 μmol/L), n = 3 independent experiments. The data are presented as mean ± SD. Multiple group comparisons were evaluated through one-way analysis of variance (ANOVA). P < 0.05 was considered statistically significant.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: Rhynchophylline rewires DLAT lipoylation via conformational control to reverse mitochondrial bioenergetic collapse against dopaminergic neuronal injury

    doi: 10.1016/j.apsb.2026.06.016

    Figure Lengend Snippet: Rhy enhances mitochondrial function by promoting mitochondrial fusion. (A) Representative fluorescent images of mitochondria stained with Mito-tracker Red in PC12 cells. (B) Quantitative analysis of mitochondrial networks in PC12 cells using the MiNA plugin for ImageJ ( n = 5 images). (C) Mitochondrial morphology in primary midbrain neurons visualized by Mito-tracker Red. (D) Mitochondrial network parameters quantified by MiNA analysis in primary midbrain neurons ( n = 5 images). (E) High-resolution imaging of mitochondrial inner membranes using PKmito Orange (PKMO) microscopy. (F) Representative transmission electron microscopy (TEM) images of mitochondrial ultrastructure. (G) Mitochondrial membrane potential quantification by JC-1 ratio (Red/Green) in PC12 cells and primary midbrain neurons, n = 3 independent experiments. (H) Cellular ATP levels determined using ATPlite™ luminescence assay ( n = 3). (I) Western blotting analysis of DRP1, p-DRP1 Ser616 , p-DRP1 Ser637 , MFN2 and OPA1 levels, following 6-OHDA (150 μmol/L) and Rhy treatment (1, 2, 5 μmol/L), n = 3 independent experiments. The data are presented as mean ± SD. Multiple group comparisons were evaluated through one-way analysis of variance (ANOVA). P < 0.05 was considered statistically significant.

    Article Snippet: Membrane were blocked with 5% non-fat milk in TBST (1 h, room temperature), and then incubated with primary antibodies (overnight, 4 °C) against DLAT (Proteintech, 13426-1-AP); DRP1 (Biodragon, RM8248); p-DRP1 Ser616 (Biodragon, BD-PP1318); p-DRP1 Ser637 (Biodragon, BD-PP0841); OPA1 (MCE, HY- P80255 ); MFN2 (Biodragon, BD-PT2740); GAPDH (Proteintech, 60004-1-Ig); TH (Santa Cruz, sc-14007); Lipoic acid (Santa Cruz, sc-101354); VMAT2 (Santa Cruz, sc-390,285); HA (Solarbio, K200003M), SIRT2 (Abways, CY5865); SIRT4(Proteintech, 66543-1-Ig); LIAS (Proteintech, 11577-1-AP); AMPK α (Biodragon, RM1159); p-AMPK α (Biodragon, RM0088); p-STAT3 (Abmart, TC52210); p-EGFR (Abmart, PC1644); KIF5B(Abclonal, A20928); KIF5C(Biodragon, BD-PN3289); KIF1B(Biodragon, BD-PN4193).

    Techniques: Staining, Imaging, Microscopy, Transmission Assay, Electron Microscopy, Membrane, Luminescence Assay, Western Blot

    DLAT mediates Rhy-induced mitochondrial fusion regulation. (A) Experimental workflow for identifying potential targets of Rhy using thermal proteome profiling (TPP) strategy. (B) Volcano plot of TPP results and screening strategy for Rhy's anti-PD targets. (C) Schematic representation of the target screening and prioritization pipeline. (D) Western blotting analysis showing Rhy-regulated mitochondrial dynamics proteins (OPA1, p-DRP1 Ser637 ) in control versus DLAT-KO cells ( n = 3). (E, F) Representative confocal images (E) and quantification (F) of mitochondrial networks visualized by Mito-tracker Red ( n = 3 fields). (G) Super-resolution microscopy images of mitochondrial cristae structures labeled with PKmito Orange (PKMO), n = 3 images. (H, I) TMRE staining reveals mitochondrial membrane potential alterations ( n = 5 fields). The data are presented as mean ± SD. Multiple group comparisons were evaluated through one-way analysis of variance (ANOVA). P < 0.05 was considered statistically significant.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: Rhynchophylline rewires DLAT lipoylation via conformational control to reverse mitochondrial bioenergetic collapse against dopaminergic neuronal injury

    doi: 10.1016/j.apsb.2026.06.016

    Figure Lengend Snippet: DLAT mediates Rhy-induced mitochondrial fusion regulation. (A) Experimental workflow for identifying potential targets of Rhy using thermal proteome profiling (TPP) strategy. (B) Volcano plot of TPP results and screening strategy for Rhy's anti-PD targets. (C) Schematic representation of the target screening and prioritization pipeline. (D) Western blotting analysis showing Rhy-regulated mitochondrial dynamics proteins (OPA1, p-DRP1 Ser637 ) in control versus DLAT-KO cells ( n = 3). (E, F) Representative confocal images (E) and quantification (F) of mitochondrial networks visualized by Mito-tracker Red ( n = 3 fields). (G) Super-resolution microscopy images of mitochondrial cristae structures labeled with PKmito Orange (PKMO), n = 3 images. (H, I) TMRE staining reveals mitochondrial membrane potential alterations ( n = 5 fields). The data are presented as mean ± SD. Multiple group comparisons were evaluated through one-way analysis of variance (ANOVA). P < 0.05 was considered statistically significant.

    Article Snippet: Membrane were blocked with 5% non-fat milk in TBST (1 h, room temperature), and then incubated with primary antibodies (overnight, 4 °C) against DLAT (Proteintech, 13426-1-AP); DRP1 (Biodragon, RM8248); p-DRP1 Ser616 (Biodragon, BD-PP1318); p-DRP1 Ser637 (Biodragon, BD-PP0841); OPA1 (MCE, HY- P80255 ); MFN2 (Biodragon, BD-PT2740); GAPDH (Proteintech, 60004-1-Ig); TH (Santa Cruz, sc-14007); Lipoic acid (Santa Cruz, sc-101354); VMAT2 (Santa Cruz, sc-390,285); HA (Solarbio, K200003M), SIRT2 (Abways, CY5865); SIRT4(Proteintech, 66543-1-Ig); LIAS (Proteintech, 11577-1-AP); AMPK α (Biodragon, RM1159); p-AMPK α (Biodragon, RM0088); p-STAT3 (Abmart, TC52210); p-EGFR (Abmart, PC1644); KIF5B(Abclonal, A20928); KIF5C(Biodragon, BD-PN3289); KIF1B(Biodragon, BD-PN4193).

    Techniques: Western Blot, Control, Super-Resolution Microscopy, Labeling, Staining, Membrane

    Rhy ameliorates mitochondrial dysfunction via suppression of the DLAT–SIRT4 axis in PD mice. (A) Representative transmission electron microscope images illustrating mitochondrial ultrastructure in substantia nigra neurons. (B, C) Protein levels of mitochondrial dynamics markers (DRP1, p-DRP1 Ser616 , p-DRP1 Ser637 , MFN2, OPA1) in SN tissues were analyzed by Western blotting ( n = 3). (D, E) Immunofluorescence co-staining demonstrating reduced DLAT–SIRT4 colocalization in substantia nigra following Rhy treatment ( n = 3). The data are presented as mean ± SD. Multiple group comparisons were evaluated through one-way analysis of variance (ANOVA). P < 0.05 was considered statistically significant.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: Rhynchophylline rewires DLAT lipoylation via conformational control to reverse mitochondrial bioenergetic collapse against dopaminergic neuronal injury

    doi: 10.1016/j.apsb.2026.06.016

    Figure Lengend Snippet: Rhy ameliorates mitochondrial dysfunction via suppression of the DLAT–SIRT4 axis in PD mice. (A) Representative transmission electron microscope images illustrating mitochondrial ultrastructure in substantia nigra neurons. (B, C) Protein levels of mitochondrial dynamics markers (DRP1, p-DRP1 Ser616 , p-DRP1 Ser637 , MFN2, OPA1) in SN tissues were analyzed by Western blotting ( n = 3). (D, E) Immunofluorescence co-staining demonstrating reduced DLAT–SIRT4 colocalization in substantia nigra following Rhy treatment ( n = 3). The data are presented as mean ± SD. Multiple group comparisons were evaluated through one-way analysis of variance (ANOVA). P < 0.05 was considered statistically significant.

    Article Snippet: Membrane were blocked with 5% non-fat milk in TBST (1 h, room temperature), and then incubated with primary antibodies (overnight, 4 °C) against DLAT (Proteintech, 13426-1-AP); DRP1 (Biodragon, RM8248); p-DRP1 Ser616 (Biodragon, BD-PP1318); p-DRP1 Ser637 (Biodragon, BD-PP0841); OPA1 (MCE, HY- P80255 ); MFN2 (Biodragon, BD-PT2740); GAPDH (Proteintech, 60004-1-Ig); TH (Santa Cruz, sc-14007); Lipoic acid (Santa Cruz, sc-101354); VMAT2 (Santa Cruz, sc-390,285); HA (Solarbio, K200003M), SIRT2 (Abways, CY5865); SIRT4(Proteintech, 66543-1-Ig); LIAS (Proteintech, 11577-1-AP); AMPK α (Biodragon, RM1159); p-AMPK α (Biodragon, RM0088); p-STAT3 (Abmart, TC52210); p-EGFR (Abmart, PC1644); KIF5B(Abclonal, A20928); KIF5C(Biodragon, BD-PN3289); KIF1B(Biodragon, BD-PN4193).

    Techniques: Transmission Assay, Microscopy, Western Blot, Immunofluorescence, Staining

    QT ameliorates the abnormal expression of OPA1 and ACSL4 proteins induced by AFB 1 . A AFB 1 with OPA1. B QT with OPA1. C AFB 1 with ACSL4. D QT with ACSL4. A – D For each panel, the left image shows the overall docking conformation, the middle image provides a magnified view of the binding site, and the right image is a two-dimensional schematic of the interaction. E and F Immunofluorescence staining and Relative fluorescence intensity of OPA1 in sheep oocyte. Scale bar: 10 μm. n = 30. G OPA1 mRNA levels in the control, AFB 1 , and AFB 1 + QT co-treatment groups. H Immunofluorescence staining of ACSL4 in sheep oocytes, Scale bar: 10 μm. I Relative fluorescence intensity values of ACSL4 in sheep oocytes. n = 30. J ACSL4 mRNA levels in the control, AFB 1 , and AFB 1 + QT co-treatment groups. a−c Values with different superscripts indicate statistical significance ( P < 0.05)

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Quercetin ameliorates aflatoxin B 1 -induced non-canonical ferroptosis in ovine oocytes through the OPA1/ACSL4 pathway

    doi: 10.1186/s40104-026-01454-3

    Figure Lengend Snippet: QT ameliorates the abnormal expression of OPA1 and ACSL4 proteins induced by AFB 1 . A AFB 1 with OPA1. B QT with OPA1. C AFB 1 with ACSL4. D QT with ACSL4. A – D For each panel, the left image shows the overall docking conformation, the middle image provides a magnified view of the binding site, and the right image is a two-dimensional schematic of the interaction. E and F Immunofluorescence staining and Relative fluorescence intensity of OPA1 in sheep oocyte. Scale bar: 10 μm. n = 30. G OPA1 mRNA levels in the control, AFB 1 , and AFB 1 + QT co-treatment groups. H Immunofluorescence staining of ACSL4 in sheep oocytes, Scale bar: 10 μm. I Relative fluorescence intensity values of ACSL4 in sheep oocytes. n = 30. J ACSL4 mRNA levels in the control, AFB 1 , and AFB 1 + QT co-treatment groups. a−c Values with different superscripts indicate statistical significance ( P < 0.05)

    Article Snippet: Oocytes were fixed in 4% paraformaldehyde for 30 min, permeabilized with immunostaining buffer for 10 min, and blocked with 2% bovine serum albumin (BSA) for 1 h. Subsequently, samples were incubated overnight at 25 °C with primary antibodies against OPA1 (1:50) (A9833, ABclonal Technology, China), ACSL4 (1:50) (A6826, ABclonal Technology, China), and FTH1 (1:50) (A25458PM, ABclonal Technology, China).

    Techniques: Expressing, Binding Assay, Immunofluorescence, Staining, Fluorescence, Control

    PRM-based verification of protein expression associated with mitochondrial function and energy metabolism. A – G Representative images showing fragment ion peak area distributions for unique peptides of OPA1 (VVVVGDQSAGK), COX15 (YQQFPEFK), FDXR (NVINTFTQTAR), HK2 (VCQIVSTR), FH (NVLHSAR), NNT (TVAELEAEK), and AK2 (APNVPAAEPVPESPK) proteins across control, AFB 1 , and AFB 1 + QT groups. H and I Log 2 fold changes for the seven proteins derived from PRO and PRM analyses, with the y -axis representing the Log 2 ratio of unique peptide relative abundance between AFB 1 + QT and AFB 1 groups ( H ), and between AFB 1 and control groups ( I ). Protein expression trends between the two treatment groups are expressed as mean values derived from PRO and PRM analyses, respectively. n = 45

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Quercetin ameliorates aflatoxin B 1 -induced non-canonical ferroptosis in ovine oocytes through the OPA1/ACSL4 pathway

    doi: 10.1186/s40104-026-01454-3

    Figure Lengend Snippet: PRM-based verification of protein expression associated with mitochondrial function and energy metabolism. A – G Representative images showing fragment ion peak area distributions for unique peptides of OPA1 (VVVVGDQSAGK), COX15 (YQQFPEFK), FDXR (NVINTFTQTAR), HK2 (VCQIVSTR), FH (NVLHSAR), NNT (TVAELEAEK), and AK2 (APNVPAAEPVPESPK) proteins across control, AFB 1 , and AFB 1 + QT groups. H and I Log 2 fold changes for the seven proteins derived from PRO and PRM analyses, with the y -axis representing the Log 2 ratio of unique peptide relative abundance between AFB 1 + QT and AFB 1 groups ( H ), and between AFB 1 and control groups ( I ). Protein expression trends between the two treatment groups are expressed as mean values derived from PRO and PRM analyses, respectively. n = 45

    Article Snippet: Oocytes were fixed in 4% paraformaldehyde for 30 min, permeabilized with immunostaining buffer for 10 min, and blocked with 2% bovine serum albumin (BSA) for 1 h. Subsequently, samples were incubated overnight at 25 °C with primary antibodies against OPA1 (1:50) (A9833, ABclonal Technology, China), ACSL4 (1:50) (A6826, ABclonal Technology, China), and FTH1 (1:50) (A25458PM, ABclonal Technology, China).

    Techniques: Expressing, Control, Derivative Assay

    QT ameliorates mitochondrial function and energy metabolism by rescuing aberrant OPA1 expression. A Representative fluorescence images of mitochondrial membrane potential (ΔΨm) in the control, AFB 1 , and AFB 1 + QT groups. Scale bar: 100 μm. B Quantification of mitochondrial membrane potential. n = 60. C Representative images depicting mitochondrial distribution patterns: (a) normal, homogeneous distribution; (b) aggregated distribution; (c) intermediate distribution; (d) distribution with low mitochondrial signal intensity. Scale bar: 10 μm. D Proportion of oocytes exhibiting normal mitochondrial distribution in the control, AFB 1 , and AFB 1 + QT groups. n = 30. E Fluorescence-based quantification of ATP levels. Scale bar: 100 μm. F Quantitative analysis of ATP content. n = 45. a−c Values with different superscripts indicate statistical significance ( P < 0.05). Data are expressed as mean ± standard error of the mean

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Quercetin ameliorates aflatoxin B 1 -induced non-canonical ferroptosis in ovine oocytes through the OPA1/ACSL4 pathway

    doi: 10.1186/s40104-026-01454-3

    Figure Lengend Snippet: QT ameliorates mitochondrial function and energy metabolism by rescuing aberrant OPA1 expression. A Representative fluorescence images of mitochondrial membrane potential (ΔΨm) in the control, AFB 1 , and AFB 1 + QT groups. Scale bar: 100 μm. B Quantification of mitochondrial membrane potential. n = 60. C Representative images depicting mitochondrial distribution patterns: (a) normal, homogeneous distribution; (b) aggregated distribution; (c) intermediate distribution; (d) distribution with low mitochondrial signal intensity. Scale bar: 10 μm. D Proportion of oocytes exhibiting normal mitochondrial distribution in the control, AFB 1 , and AFB 1 + QT groups. n = 30. E Fluorescence-based quantification of ATP levels. Scale bar: 100 μm. F Quantitative analysis of ATP content. n = 45. a−c Values with different superscripts indicate statistical significance ( P < 0.05). Data are expressed as mean ± standard error of the mean

    Article Snippet: Oocytes were fixed in 4% paraformaldehyde for 30 min, permeabilized with immunostaining buffer for 10 min, and blocked with 2% bovine serum albumin (BSA) for 1 h. Subsequently, samples were incubated overnight at 25 °C with primary antibodies against OPA1 (1:50) (A9833, ABclonal Technology, China), ACSL4 (1:50) (A6826, ABclonal Technology, China), and FTH1 (1:50) (A25458PM, ABclonal Technology, China).

    Techniques: Expressing, Fluorescence, Membrane, Control

    Inhibition of AFB 1 -induced aberrant OPA1 and ACSL4 expression alleviates ferroptosis in sheep oocytes. A – F LPO fluorescence signals ( A ), comparative fluorescence intensity of LPO ( B ), fluorescence signals of Fe 2+ ( C ), fluorescence intensity of Fe 2+ ( D ), fluorescence signals of Annexin-V ( E ), and fluorescence intensity of Annexin-V ( F ) in ovine oocytes within various treatment groups. Scale bar: 10 μm. G Examination of mitochondrial ultrastructure in ovine oocytes from each category. Green arrows indicate mitochondrial cristae; yellow arrows highlight abnormal structures of the mitochondrial membrane; red arrows denote the absence of mitochondrial cristae. Scale bar: 200 nm. a,b Values with different superscripts indicate statistical significance ( P < 0.05)

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Quercetin ameliorates aflatoxin B 1 -induced non-canonical ferroptosis in ovine oocytes through the OPA1/ACSL4 pathway

    doi: 10.1186/s40104-026-01454-3

    Figure Lengend Snippet: Inhibition of AFB 1 -induced aberrant OPA1 and ACSL4 expression alleviates ferroptosis in sheep oocytes. A – F LPO fluorescence signals ( A ), comparative fluorescence intensity of LPO ( B ), fluorescence signals of Fe 2+ ( C ), fluorescence intensity of Fe 2+ ( D ), fluorescence signals of Annexin-V ( E ), and fluorescence intensity of Annexin-V ( F ) in ovine oocytes within various treatment groups. Scale bar: 10 μm. G Examination of mitochondrial ultrastructure in ovine oocytes from each category. Green arrows indicate mitochondrial cristae; yellow arrows highlight abnormal structures of the mitochondrial membrane; red arrows denote the absence of mitochondrial cristae. Scale bar: 200 nm. a,b Values with different superscripts indicate statistical significance ( P < 0.05)

    Article Snippet: Oocytes were fixed in 4% paraformaldehyde for 30 min, permeabilized with immunostaining buffer for 10 min, and blocked with 2% bovine serum albumin (BSA) for 1 h. Subsequently, samples were incubated overnight at 25 °C with primary antibodies against OPA1 (1:50) (A9833, ABclonal Technology, China), ACSL4 (1:50) (A6826, ABclonal Technology, China), and FTH1 (1:50) (A25458PM, ABclonal Technology, China).

    Techniques: Inhibition, Expressing, Fluorescence, Membrane

    QT suppresses AFB 1 -induced iron-dependent non-canonical ferroptosis in oocytes via the OPA1/ACSL4 pathway. A Molecular docking analysis results for the OPA1 and ACSL4 interaction. The left panel shows the overall docking conformation; the right panel provides a magnified view of the binding site. Red dashed lines indicate hydrogen bonds, with adjacent numbers denoting bond lengths. Effective hydrogen bond lengths fall within the 1.5–3.5 Å range; within this interval, a shorter bond length indicates greater amino acid residue criticality. Amino acid residues connected by the red dashed lines represent interaction sites; yellow indicates residues from the OPA1 protein, purple indicates residues from the ACSL4 protein. B – J OPA1 , ACSL4 , NCOA4 , FTH1 , SLC11A2 , CAT , GPX7 , TP53 and BCL2/BAX mRNA levels across different treatment groups

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Quercetin ameliorates aflatoxin B 1 -induced non-canonical ferroptosis in ovine oocytes through the OPA1/ACSL4 pathway

    doi: 10.1186/s40104-026-01454-3

    Figure Lengend Snippet: QT suppresses AFB 1 -induced iron-dependent non-canonical ferroptosis in oocytes via the OPA1/ACSL4 pathway. A Molecular docking analysis results for the OPA1 and ACSL4 interaction. The left panel shows the overall docking conformation; the right panel provides a magnified view of the binding site. Red dashed lines indicate hydrogen bonds, with adjacent numbers denoting bond lengths. Effective hydrogen bond lengths fall within the 1.5–3.5 Å range; within this interval, a shorter bond length indicates greater amino acid residue criticality. Amino acid residues connected by the red dashed lines represent interaction sites; yellow indicates residues from the OPA1 protein, purple indicates residues from the ACSL4 protein. B – J OPA1 , ACSL4 , NCOA4 , FTH1 , SLC11A2 , CAT , GPX7 , TP53 and BCL2/BAX mRNA levels across different treatment groups

    Article Snippet: Oocytes were fixed in 4% paraformaldehyde for 30 min, permeabilized with immunostaining buffer for 10 min, and blocked with 2% bovine serum albumin (BSA) for 1 h. Subsequently, samples were incubated overnight at 25 °C with primary antibodies against OPA1 (1:50) (A9833, ABclonal Technology, China), ACSL4 (1:50) (A6826, ABclonal Technology, China), and FTH1 (1:50) (A25458PM, ABclonal Technology, China).

    Techniques: Binding Assay, Residue

    ( A to Db ) Cross sections through the Gas muscle of Pax +/+ , Myh7 fl/+ (A to Bb) and Pax7 icre/+ , Myh7 Δ/fl (C to Db) mice at 2 and 12 months, respectively, labeled by immunofluorescence for MyHC-slow (green), troponin T1 (red), and DAPI (blue). Scale bars, 100 μm (Cb and Db). ( E to H ) SDH staining on Gas muscle sections of Pax +/+ , Myh7 fl/+ (E and G) and Pax7 icre/+ , Myh7 Δ/fl (Ea and Ga) mice and quantification of the percentage SDH activity (F and H) at 2 and 12 months of age, respectively ( n = 5). Scale bars, 100 μm (Ea and Ga). ( I to L ) Representative Western blots for troponin T1, PGC-1α, and α-tubulin (loading control) using Gas muscle protein lysates of Pax +/+ , Myh7 fl/+ , Pax3 cre/+ , Myh7 Δ/fl (P0), and Pax7 icre/+ , Myh7 Δ/fl mice at P0 and 2 and 6 months (I) and their densitometric quantification (J to L) ( n = 4). ( M to P ) Representative Western blots for mitochondrial complexes and α-tubulin (loading control) using protein lysates from the Gas muscle of Pax +/+ , Myh7 fl/+ , Pax3 cre/+ , Myh7 Δ/fl (P0), and Pax7 icre/+ , Myh7 Δ/fl mice at P0 and 6 months (M and O) and their densitometric quantification (N to P) ( n = 4 to 6). ( Q to T ) Representative Western blots for FIS1, pDRP1, DRP1, OPA1, Mitofusin 1, Mitofusin 2, and α-tubulin (loading control) using protein lysates from the Gas muscle of Pax +/+ , Myh7 fl/+ , Pax3 cre/+ , Myh7 Δ/fl (P0), and Pax7 icre/+ , Myh7 Δ/fl mice at P0 and 2 and 6 months (Q) and densitometric quantification (R to T) ( n = 4). ( U and V ) Quantification of ATP levels in the Gas muscle of Pax +/+ , Myh7 fl/+ and Pax7 icre/+ , Myh7 Δ/fl mice at 2 and 12 months of age ( n = 5). Data are presented as means ± SEM. * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.

    Journal: Science Advances

    Article Title: The skeletal muscle slow myosin heavy chain regulates mammalian metabolic homeostasis through the NRF2 pathway

    doi: 10.1126/sciadv.aed2478

    Figure Lengend Snippet: ( A to Db ) Cross sections through the Gas muscle of Pax +/+ , Myh7 fl/+ (A to Bb) and Pax7 icre/+ , Myh7 Δ/fl (C to Db) mice at 2 and 12 months, respectively, labeled by immunofluorescence for MyHC-slow (green), troponin T1 (red), and DAPI (blue). Scale bars, 100 μm (Cb and Db). ( E to H ) SDH staining on Gas muscle sections of Pax +/+ , Myh7 fl/+ (E and G) and Pax7 icre/+ , Myh7 Δ/fl (Ea and Ga) mice and quantification of the percentage SDH activity (F and H) at 2 and 12 months of age, respectively ( n = 5). Scale bars, 100 μm (Ea and Ga). ( I to L ) Representative Western blots for troponin T1, PGC-1α, and α-tubulin (loading control) using Gas muscle protein lysates of Pax +/+ , Myh7 fl/+ , Pax3 cre/+ , Myh7 Δ/fl (P0), and Pax7 icre/+ , Myh7 Δ/fl mice at P0 and 2 and 6 months (I) and their densitometric quantification (J to L) ( n = 4). ( M to P ) Representative Western blots for mitochondrial complexes and α-tubulin (loading control) using protein lysates from the Gas muscle of Pax +/+ , Myh7 fl/+ , Pax3 cre/+ , Myh7 Δ/fl (P0), and Pax7 icre/+ , Myh7 Δ/fl mice at P0 and 6 months (M and O) and their densitometric quantification (N to P) ( n = 4 to 6). ( Q to T ) Representative Western blots for FIS1, pDRP1, DRP1, OPA1, Mitofusin 1, Mitofusin 2, and α-tubulin (loading control) using protein lysates from the Gas muscle of Pax +/+ , Myh7 fl/+ , Pax3 cre/+ , Myh7 Δ/fl (P0), and Pax7 icre/+ , Myh7 Δ/fl mice at P0 and 2 and 6 months (Q) and densitometric quantification (R to T) ( n = 4). ( U and V ) Quantification of ATP levels in the Gas muscle of Pax +/+ , Myh7 fl/+ and Pax7 icre/+ , Myh7 Δ/fl mice at 2 and 12 months of age ( n = 5). Data are presented as means ± SEM. * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.

    Article Snippet: The antibodies used for Western blotting were as follows: anti-mouse MyHC-IIa antibody (SC-71, Developmental Studies Hybridoma Bank) at 1:10 dilution; anti-mouse MyHC-IIb antibody (BFF3, Developmental Studies Hybridoma Bank) at 1:10; anti-mouse alpha-tubulin antibody (30021290, Cell Signaling Technology) at 1:10,000; anti-rabbit GAPDH antibody (PAB932Mu01, Cloud-Clone Corp) at 1:10,000; anti-rabbit Akt antibody (4641, Cell Signaling Technology) at 1:1000; anti-rabbit P-Akt S473 (4640, Cell Signaling Technology) at 1:1000; anti-rabbit Histone H3 antibody (Ab1741, Abcam) at 1:10,000; anti-rabbit troponin T1 antibody (NBP238855, Novus Biologicals) at 1:5000; anti-rabbit PGC-1α antibody (A12348, ABclonal; 66369, Proteintech; and 2178S, Cell Signaling Technology) at 1:2000, 1:2000, and 1:1000, respectively; anti-mouse total OXPHOS cocktail (ab110413, Abcam) at 1:1000; anti-rabbit DRP1 antibody (A21968, ABclonal) at 1:2000; anti-rabbit FIS1 antibody (A19666, ABclonal) at 1:2000; anti-rabbit mitofusin1 antibody (A9880, ABclonal) at 1:2000; anti-rabbit mitofusin2 antibody (A12771, ABclonal) at 1:2000; anti-rabbit GLUT4 (MA5-17176, Thermo Fisher Scientific) at 1:1000; anti-rabbit NRF2 antibody (A0674, ABclonal and 98020000, Proteintech) at 1:2000; anti-rabbit P-NRF2 antibody (AP1133, ABclonal) at 1:2000; anti-rabbit SOD1 antibody (A0274, ABclonal) at 1:2000; anti-rabbit Prdx1 antibody (A13524, ABclonal) at 1:2000; anti-rabbit Gpx1 antibody (A1110, ABclonal) at 1:1000; anti-rabbit catalase antibody (A11220, ABclonal) at 1:2000; anti-rabbit KEAP1 antibody (A1820, ABclonal) at 1:1000; anti-rabbit Tom20 antibody (HPA011582, Merck) at 1:2500, anti-rabbit VDAC1 antibody ( Ab154856 , Abcam) at 1:2500; anti-rabbit pDRP1 (S616) antibody (AP0849, ABclonal) at 1:2500; and anti-rabbit OPA1 antibody (A9833, ABclonal) at 1:2500.

    Techniques: Labeling, Immunofluorescence, Staining, Activity Assay, Western Blot, Control

    COPN restores mitochondrial quality control and interrupts the ROS‒cGAS‒inflammation axis in OGD/R-treated R28 cells. a , TEM images showing changes in the mitochondrial ultrastructure of R28 cells subjected to various treatments (PBS, PDNs, COPN-L, and COPN-H) after OGD/R. Scale bar: 500 nm b , Quantitative analyses of mitochondrial length and number in R28 cells as indicated in a . c , Representative fluorescence images showing JC-1 staining of the mitochondrial Δψm: aggregates (red) indicate healthy mitochondria, whereas monomers (green) represent depolarized mitochondria. Nuclei were stained with DAPI (blue). Scale bar: 50 μm d , Intracellular ATP content assay revealing improved energy production after COPN treatment under OGD/R stress conditions. e , mRNA expression analysis of mitochondrial dynamic regulatory genes (Opa1, Mfn2, Drp1, and Fis1) and mitochondrial DNA transcription levels (mt-ND1 and mt-COX1). f , Quantitative analysis of the JC-1 fluorescence ratio (aggregates/monomers) and mitochondrial ROS levels (MitoSOX staining). g–h , Western blot analysis of proteins involved in mitochondrial autophagy (Pink1, Parkin, and P62) (g) and mitochondrial fusion/fission (Opa1, Mfn2, Mfn1, Drp1, and Fis1) (h) . i , Confocal fluorescence microscopy images of mitochondria (green, MitoTracker) and lysosomes (red, LysoTracker) in R28 cells after different treatments. Nuclei were stained with Hoechst (blue). Scale bar: 50 μm ∗ ∗∗∗P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Journal: Materials Today Bio

    Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

    doi: 10.1016/j.mtbio.2026.102974

    Figure Lengend Snippet: COPN restores mitochondrial quality control and interrupts the ROS‒cGAS‒inflammation axis in OGD/R-treated R28 cells. a , TEM images showing changes in the mitochondrial ultrastructure of R28 cells subjected to various treatments (PBS, PDNs, COPN-L, and COPN-H) after OGD/R. Scale bar: 500 nm b , Quantitative analyses of mitochondrial length and number in R28 cells as indicated in a . c , Representative fluorescence images showing JC-1 staining of the mitochondrial Δψm: aggregates (red) indicate healthy mitochondria, whereas monomers (green) represent depolarized mitochondria. Nuclei were stained with DAPI (blue). Scale bar: 50 μm d , Intracellular ATP content assay revealing improved energy production after COPN treatment under OGD/R stress conditions. e , mRNA expression analysis of mitochondrial dynamic regulatory genes (Opa1, Mfn2, Drp1, and Fis1) and mitochondrial DNA transcription levels (mt-ND1 and mt-COX1). f , Quantitative analysis of the JC-1 fluorescence ratio (aggregates/monomers) and mitochondrial ROS levels (MitoSOX staining). g–h , Western blot analysis of proteins involved in mitochondrial autophagy (Pink1, Parkin, and P62) (g) and mitochondrial fusion/fission (Opa1, Mfn2, Mfn1, Drp1, and Fis1) (h) . i , Confocal fluorescence microscopy images of mitochondria (green, MitoTracker) and lysosomes (red, LysoTracker) in R28 cells after different treatments. Nuclei were stained with Hoechst (blue). Scale bar: 50 μm ∗ ∗∗∗P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Article Snippet: The following primary antibodies were used: Drp1 (CST, #8570, 1:1000, ∼80 kDa), Fis1 (Proteintech, 10956-1-AP, 1:1000, ∼17 kDa), Mfn1 (Abcam, ab104274, 1:1000, ∼84 kDa), Mfn2 (CST, #9482, 1:1000, ∼86 kDa), Opa1 (CST, #80471, 1:1000, ∼100–120 kDa), Pink1 (CST, #6946, 1:1000, ∼63 kDa), cGAS (CST, #15102, 1:1000, ∼60 kDa), STING (CST, #13647, 1:1000, ∼42–45 kDa), TBK1 (CST, #3013, 1:1000, ∼84 kDa), p-TBK1 (CST, #5483, 1:1000, ∼84 kDa), COX IV (Abcam, ab14744, 1:2000, ∼17 kDa), β-actin (Proteintech, 66009-1-Ig, 1:5000, ∼43 kDa), and GAPDH (Proteintech, 60004-1-Ig, 1:5000, After washing, the membranes were incubated with HRP-conjugated secondary antibodies (goat anti-rabbit or goat anti-mouse IgG, CST, 1:5000) for 1 h at room temperature.

    Techniques: Control, Fluorescence, Staining, Expressing, Western Blot, Microscopy