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anti 4 hydroxynonenal 4 hne antibody (R&D Systems)

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R&D Systems anti 4 hydroxynonenal 4 hne antibody
Anti 4 Hydroxynonenal 4 Hne Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 365 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+4+hne+antibody/4-Hydroxynonenal+Antibody/pm41986303-232-21-25
Average 96 stars, based on 365 article reviews

anti 4 hydroxynonenal 4 hne antibody - by Bioz Stars, 2026-10

96/100 stars

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Article Title: Iron supplementation alleviates pathologies in a mouse model of facioscapulohumeral muscular dystrophy
Article Snippet: Mouse anti–myosin heavy chain (anti-MyHC) antibody (MF20; 1:5 for IF) was obtained from the Developmental Studies Hybridoma Bank.

Article Title: The Gpx4NIKO Mouse Is a Versatile Model for Testing Interventions Targeting Ferroptotic Cell Death of Spinal Motor Neurons.
Article Snippet: Antibodies used: Anti-NeuN (MAB377, Millipore, Billerica, Massachusetts); anti-ChAT, Anti-PSD95, anti-Actin, anti-GFAP (Cell Signaling Technology, Beverly, MA); antiGAPDH (Sigma-Aldrich, St. Louis, MO); anti-Iba-1 (Wako Chemicals USA, VA); anti-4-HNE antibody from R&D Systems (Minneapolis, MN); and anti-GPX4 (Santa Cruz Biotechnology, CA).

Article Title: Effect of allyl isothiocyanate on 4-HNE induced glucocorticoid resistance in COPD and the underlying mechanism
Article Snippet: The anti-HDAC2 antibody was purchased from Abcam (Cambridge, UK), and the anti-4-HNE antibody was obtained from R&D Systems (USA).

Article Title: Selenized Tripterine Phytosomes Alleviate Ferroptosis-Mediated Acute Kidney Injury by Suppressing GPX4 Degradation via the DUSP1/Autophagy Pathway
Article Snippet: The anti-4-HNE antibody was a product of R&D Systems (Emeryville, CA, USA).

Article Title: Glycogen Synthase Kinase 3 β Hepatocyte Deletion Attenuates Ferroptosis and Metabolic Dysfunction-associated Steatohepatitis in Mice
Article Snippet: The primary antibodies employed in the study include anti-α-SMA (ab124964) from Abcam, anti- glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (MAB374) from Millipore Sigma, anti-MPO (#AF3667) from R&D systems, anti-nicotinamide phosphoribosyl transferase (NAMPT) (#A11776-1-AP) from Proteintech, anti-F4/80 (#70076S) from Cell Signaling Technology, anti-4-HNE antibody (MAB3249), and human/mouse/rat GPX4 (h/m/rGPX4) antibody (MAB5457) from R&D Systems, anti-oxidized phospholipid (oxPAPC) antibody (MABS2278) from Sigma-Aldrich (Merck KGaA), anti-TFRC antibody (ab214039) from Abcam, hyperoxidized peroxiredoxin-3 polyclonal (SO 2/3 -PRDX3) antibody (#39806) from Cayman Chemical, GS antibody (#G2781) from Sigma-Aldrich, CYP2F2 (#sc-374540) antibody from Santa Cruz Biotechnology, vinculin (7F9) antibody (#sc-73614) from Santa Cruz, and Cit-Histone H3 (Arg2, Arg8, Arg17) polyclonal (#630-180) antibody from ThermoFisher.

Incubation:

Article Title: Hwangkeumjakyak-tang protects against hepatocyte damage via oxidative stress inhibition and affects the altered gut microbiome pattern in acetaminophen-induced liver injury
Article Snippet: .. Briefly, deparaffinized tissue sections were incubated with monoclonal anti-4-HNE antibody (R&D Systems, Minneapolis, MN, USA). .. Stained sections were examined using a Motic Easyscan Digital Slide Scanner (Motic, Hong Kong, China).

Article Title: Ubiquitin-specific protease 20(USP20) mitigates doxorubicin-induced cardiotoxicity by deubiquitinating and stabilizing HuR.
Article Snippet: The severe cardiotoxicity of doxorubicin (Dox) significantly restricts its clinical application.. Deubiquitinating enzymes (DUBs) have emerged as a research hotspot in cardiac pathophysiology due to their precise regulation of protein function, localization, and degradation.. However, the specific role of ubiquitin-specific peptidase 20 (USP20) in doxorubicin-induced cardiomyopathy (DIC) remains poorly understood.

Western Blot:

Article Title: The Gpx4NIKO mouse is a versatile model for testing interventions targeting ferroptotic cell death of spinal motor neurons
Article Snippet: .. Antibodies and Western blots Antibodies used: Anti-NeuN (MAB377, Millipore, Billerica, Massachusetts); anti-ChAT, Anti-PSD95, anti-Actin, anti-GFAP (Cell Signaling Technology, Beverly, MA); anti-GAPDH (Sigma-Aldrich, St. Louis, MO); anti-Iba-1 (Wako Chemicals USA, VA); anti-4-HNE antibody from R&D Systems (Minneapolis, MN); and anti-GPX4 (Santa Cruz Biotechnology, CA). ..

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ADGRG1 have the capacity to serve as potential target for IVDD treatment. (A) Primary human NPCs were treated with TBHP at concentrations of 50 μM, 100 μM, 200 μM for 12 h, and the cellular ferrous ion levels were assessed by confocal microscopy using FerroOrange probe. FerroOrange fluorescence intensity was quantified, n = 3. Scale bar, 50 μm. (B) GSEA enrichment plots of gene data sets associated with oxidative damage response, ferroptosis, permeabilize mitochondria and mitochondrial respiratory chain complex assembly in TBHP‐treated primary NPCs, compared to the control. (C) Primary NPCs were treated with TBHP for 12 h and cell lysates were subjected to immunoblotting with indicated ADGRG1, IVDD and ferroptosis-related antibodies. (D) Volcano plot of differentially expressed genes in NPCs between the TBHP‐treated group and the control. |log2FC| > 2, FDR < 0.05. (E-F) Primary NPCs were incubated with TBHP for 12 h, followed by immunofluorescent staining with anti-ADGRG1 (green) and anti-4-HNE (red) antibodies and examination by confocal microscopy. The fluorescence intensity was quantified. n = 3. Scale bar, 50 μm. (G) Magnetic resonance imaging (MRI) showed the IVDD Pfirrmann grade of needle puncture IVDD rat models with 25G (MI-IVDD), 21G(MOD-IVDD) and18G (SE-IVDD), and statistical analysis was performed, n = 3. (H) Immunoblotting analysis showed the expression of IVDD markers (COL1A1) and ADGRG1 in IVDD rat models with different degrees of needle-puncture degeneration, n = 3. (I) Feature plots depict the average expression of ADGRG1 (color-scaled) across each cell cluster. (J) Immunoblotting analysis showed the expression of IVDD markers (COL1A1) and ADGRG1 in the NP tissue of clinical MI/SE degenerative IVDs. The relative ADGRG1 grayscale was quantified in (L), n = 10. (K) Representative images for colocalization analysis of ADGRG1 (green), 4-HNE (red) fluorescence in MI and SE NP tissues. n = 5. Scale bar, 50 μm. (L) Relative ADGRG1 grayscale in (J) and fluorescence intensity in (K) were quantified. All data are expressed as the mean ± SD. For panels A) and F–H), data were analyzed using one-way ANOVA with Tukey's multiple comparisons, while panel L) was assessed using a two-tailed unpaired Student's t-test. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001.

Journal: Bioactive Materials

Article Title: ADGRG1-targeted hypoxia preconditioned extracellular vesicles ameliorate intervertebral disc degeneration by delivering taurine to disrupt the oxidative stress feedback loop-driven ferroptosis in nucleus pulposus cells

doi: 10.1016/j.bioactmat.2026.02.029

Figure Lengend Snippet: ADGRG1 have the capacity to serve as potential target for IVDD treatment. (A) Primary human NPCs were treated with TBHP at concentrations of 50 μM, 100 μM, 200 μM for 12 h, and the cellular ferrous ion levels were assessed by confocal microscopy using FerroOrange probe. FerroOrange fluorescence intensity was quantified, n = 3. Scale bar, 50 μm. (B) GSEA enrichment plots of gene data sets associated with oxidative damage response, ferroptosis, permeabilize mitochondria and mitochondrial respiratory chain complex assembly in TBHP‐treated primary NPCs, compared to the control. (C) Primary NPCs were treated with TBHP for 12 h and cell lysates were subjected to immunoblotting with indicated ADGRG1, IVDD and ferroptosis-related antibodies. (D) Volcano plot of differentially expressed genes in NPCs between the TBHP‐treated group and the control. |log2FC| > 2, FDR < 0.05. (E-F) Primary NPCs were incubated with TBHP for 12 h, followed by immunofluorescent staining with anti-ADGRG1 (green) and anti-4-HNE (red) antibodies and examination by confocal microscopy. The fluorescence intensity was quantified. n = 3. Scale bar, 50 μm. (G) Magnetic resonance imaging (MRI) showed the IVDD Pfirrmann grade of needle puncture IVDD rat models with 25G (MI-IVDD), 21G(MOD-IVDD) and18G (SE-IVDD), and statistical analysis was performed, n = 3. (H) Immunoblotting analysis showed the expression of IVDD markers (COL1A1) and ADGRG1 in IVDD rat models with different degrees of needle-puncture degeneration, n = 3. (I) Feature plots depict the average expression of ADGRG1 (color-scaled) across each cell cluster. (J) Immunoblotting analysis showed the expression of IVDD markers (COL1A1) and ADGRG1 in the NP tissue of clinical MI/SE degenerative IVDs. The relative ADGRG1 grayscale was quantified in (L), n = 10. (K) Representative images for colocalization analysis of ADGRG1 (green), 4-HNE (red) fluorescence in MI and SE NP tissues. n = 5. Scale bar, 50 μm. (L) Relative ADGRG1 grayscale in (J) and fluorescence intensity in (K) were quantified. All data are expressed as the mean ± SD. For panels A) and F–H), data were analyzed using one-way ANOVA with Tukey's multiple comparisons, while panel L) was assessed using a two-tailed unpaired Student's t-test. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001.

Article Snippet: After permeabilization and blocking with 10% goat serum containing 0.2% Triton X-100, the sections were incubated with primary antibodies against ADGRG1 (1:50; sc-390192, Santa Cruz Biotechnology), TOM20(11802-1-AP, Proteintech), 4-HNE(68538-1-Ig, Proteintech), 4-HNE(HY-P81208, MCE), Ferritin (Rockland 200-401-090-0100), LAMP1(65051-1-Ig, Proteintech), PAX1(sc-514352, Santa Cruz Biotechnology), FOXF1(PA5-83039, Thermo Fisher).

Techniques: Confocal Microscopy, Fluorescence, Control, Western Blot, Incubation, Staining, Magnetic Resonance Imaging, Expressing, Two Tailed Test

In vitro evaluation of the cargo transfer capacity and therapeutic potential of A1TP-HX-EVs. (A) Immunoblotting analysis confirmed the overexpression of GFP-tagged ADGEG1 protein in NPCs by retrovirus. (B) The live-cell workstation demonstrated the uptake of AIE-labeled A1TP-HX-EVs by NPCs in both the control group (GFP) and the ADGRG1 overexpression group (ADGRG1-GFP) within 24 h. (C) Representative images from the live-cell workstation showed the uptake of DPA-labeled HX-EVs at different concentrations by TBHP-treated NPCs within 24 h. Scale bar, 50 μm. (D) Representative images from the live-cell workstation showed the uptake of AIE-labeled A1TP-HX-EVs (DPA 10 μM) by primary NPCs within 24 h after treatment with different concentrations of TBHP for 12h. Scale bar, 50 μm. (E) AIE fluorescence intensity in (C-D) were quantified. n = 3. ∗ P < 0.05. ∗∗ P < 0.01. ns, not significant. (F) Primary NPCs were stained with FerroOrange probe and assessed by confocal microscopy. n = 3. Scale bar, 50 μm. (G) GSEA enrichment analysis of ferroptosis and oxidative damage response-related gene sets in A1TP-HX-EVs‐treated group and TBHP group NPCs. (H) Primary NPCs were induced with 100 μM TBHP for 12 h, and then treated with EVs, HX-EVs or A1TP-HX-EVs for 24 h. Cell lysates were immunoblotted with antibodies against IVDD markers and ferroptosis-related proteins and ADGRG1. (I) GSEA enrichment analysis of the mitochondrial respiratory chain complex assembly and transcriptional activation of mitochondrial biogenesis-related gene sets in A1TP-HX-EVs‐treated group and TBHP group NPCs. (J-K) Representative oxygen consumption traces of primary NPCs induced with TBHP and then treated as indicated for 24 h. Maximal respiration of NPCs were quantified. n = 3. (L) Primary NPCs were induced with TBHP, and then treated as indicated for 24 h, followed by immunofluorescent staining with anti-TOM20 (green) and anti-4-HNE (red) antibodies. n = 3. Scale bar, 50 μm. All data are expressed as the mean ± SD. For B) and E), two‐way ANOVA with Tukey 's multiple comparison tests were used for statistical analysis. For panels F) and K-L), one‐way ANOVA with Tukey's multiple comparison tests were used for statistical analysis. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001. ns, not significant.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.029

Figure Lengend Snippet: In vitro evaluation of the cargo transfer capacity and therapeutic potential of A1TP-HX-EVs. (A) Immunoblotting analysis confirmed the overexpression of GFP-tagged ADGEG1 protein in NPCs by retrovirus. (B) The live-cell workstation demonstrated the uptake of AIE-labeled A1TP-HX-EVs by NPCs in both the control group (GFP) and the ADGRG1 overexpression group (ADGRG1-GFP) within 24 h. (C) Representative images from the live-cell workstation showed the uptake of DPA-labeled HX-EVs at different concentrations by TBHP-treated NPCs within 24 h. Scale bar, 50 μm. (D) Representative images from the live-cell workstation showed the uptake of AIE-labeled A1TP-HX-EVs (DPA 10 μM) by primary NPCs within 24 h after treatment with different concentrations of TBHP for 12h. Scale bar, 50 μm. (E) AIE fluorescence intensity in (C-D) were quantified. n = 3. ∗ P < 0.05. ∗∗ P < 0.01. ns, not significant. (F) Primary NPCs were stained with FerroOrange probe and assessed by confocal microscopy. n = 3. Scale bar, 50 μm. (G) GSEA enrichment analysis of ferroptosis and oxidative damage response-related gene sets in A1TP-HX-EVs‐treated group and TBHP group NPCs. (H) Primary NPCs were induced with 100 μM TBHP for 12 h, and then treated with EVs, HX-EVs or A1TP-HX-EVs for 24 h. Cell lysates were immunoblotted with antibodies against IVDD markers and ferroptosis-related proteins and ADGRG1. (I) GSEA enrichment analysis of the mitochondrial respiratory chain complex assembly and transcriptional activation of mitochondrial biogenesis-related gene sets in A1TP-HX-EVs‐treated group and TBHP group NPCs. (J-K) Representative oxygen consumption traces of primary NPCs induced with TBHP and then treated as indicated for 24 h. Maximal respiration of NPCs were quantified. n = 3. (L) Primary NPCs were induced with TBHP, and then treated as indicated for 24 h, followed by immunofluorescent staining with anti-TOM20 (green) and anti-4-HNE (red) antibodies. n = 3. Scale bar, 50 μm. All data are expressed as the mean ± SD. For B) and E), two‐way ANOVA with Tukey 's multiple comparison tests were used for statistical analysis. For panels F) and K-L), one‐way ANOVA with Tukey's multiple comparison tests were used for statistical analysis. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001. ns, not significant.

Techniques: In Vitro, Western Blot, Over Expression, Labeling, Control, Fluorescence, Staining, Confocal Microscopy, Activation Assay, Comparison

Taurine is the key small molecule in A1TP-HX-EVs that activated the AMPK/NRF2 pathway to regulate nucleus pulposus cell repair. (A) The LC-MS/MS analysis was used to detect the differential active small molecule components between placental HX-EVs and EVs. (B) The SMPDB enrichment analysis identified pathways related to small molecules that are up-expressed in HX-EVs compared to EVs. The metabolic pathways marked in red are related to ferroptosis inhibition and mitochondrial function. (C) Volcano plot of small molecule in HX-EVs versus EVs. |log2FC| > 0.5, FDR <0.05. (D) The content of taurine in placental MSC (pMSC), hypoxia-induced pMSC(HX-pMSC) and their derived EVs was detected by ELISA. n = 3. (E) Primary NPCs cells were induced with TBHP, and then treated with EVs, HX-EVs, and A1TP-HX-EVs for 24 h. The cell lysates were subjected to ELISA assay to detect taurine content. (F) Two shRNA lentiviruses were designed to knock down TAUT a key enzyme in taurine uptake in pMSC. (G) The content of taurine in TAUT-sh1-pMSC and TAUT-sh2-pMSC derived EVs (KD-HX-EVs) was detected by ELISA. n = 3. (H) Primary NPCs were induced with TBHP, and then treated with A1TP-HX-EVs and A1TP-KD-HX-EVs for 24 h. Cell lysates were immunoblotted with indicated antibodies. (I) Primary NPCs were induced with TBHP, and then treated with A1TP-HX-EVs and A1TP-KD-HX-EVs for 24 h, followed by immunofluorescent staining with anti- TOM20 (green) and anti-4-HNE (red) antibodies. n = 3. Scale bar, 50 μm. (J) A CDO1-overexpressing retrovirus was designed to overexpress CDO1 in pMSCs. (K) The content of taurine in CDO1-OE-pMSC derived EVs (OE-EVs) was detected by ELISA. n = 3. (L) Primary NPCs were induced with TBHP, and then treated with treated A1TP-EVs and A1TP-OE-EVs for 24 h. Cell lysates were immunoblotted with indicated antibodies. (M) Primary NPCs were induced with TBHP, and then treated with A1TP-EVs and A1TP-OE-EVs for 24 h, followed by immunofluorescent staining with anti-TOM20 (green) and anti-4-HNE (red) antibodies. n = 3. Scale bar, 50 μm. (N-O) Representative oxygen consumption traces of primary NPCs induced with TBHP and then treated with A1TP-HX-EVs, A1TP-KD-HX-EVs, or A1TP-OE-EVs for 24 h. Maximal respiration of NPCs were quantified. n = 3. All data are expressed as the mean ± SD. For E), I), M) and O), one‐way ANOVA with Tukey's multiple comparison tests were used for statistical analysis. For D), G) and K), two‐tailed unpaired Student's t‐tests were used for statistical analysis. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001. ns, not significant.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.029

Figure Lengend Snippet: Taurine is the key small molecule in A1TP-HX-EVs that activated the AMPK/NRF2 pathway to regulate nucleus pulposus cell repair. (A) The LC-MS/MS analysis was used to detect the differential active small molecule components between placental HX-EVs and EVs. (B) The SMPDB enrichment analysis identified pathways related to small molecules that are up-expressed in HX-EVs compared to EVs. The metabolic pathways marked in red are related to ferroptosis inhibition and mitochondrial function. (C) Volcano plot of small molecule in HX-EVs versus EVs. |log2FC| > 0.5, FDR <0.05. (D) The content of taurine in placental MSC (pMSC), hypoxia-induced pMSC(HX-pMSC) and their derived EVs was detected by ELISA. n = 3. (E) Primary NPCs cells were induced with TBHP, and then treated with EVs, HX-EVs, and A1TP-HX-EVs for 24 h. The cell lysates were subjected to ELISA assay to detect taurine content. (F) Two shRNA lentiviruses were designed to knock down TAUT a key enzyme in taurine uptake in pMSC. (G) The content of taurine in TAUT-sh1-pMSC and TAUT-sh2-pMSC derived EVs (KD-HX-EVs) was detected by ELISA. n = 3. (H) Primary NPCs were induced with TBHP, and then treated with A1TP-HX-EVs and A1TP-KD-HX-EVs for 24 h. Cell lysates were immunoblotted with indicated antibodies. (I) Primary NPCs were induced with TBHP, and then treated with A1TP-HX-EVs and A1TP-KD-HX-EVs for 24 h, followed by immunofluorescent staining with anti- TOM20 (green) and anti-4-HNE (red) antibodies. n = 3. Scale bar, 50 μm. (J) A CDO1-overexpressing retrovirus was designed to overexpress CDO1 in pMSCs. (K) The content of taurine in CDO1-OE-pMSC derived EVs (OE-EVs) was detected by ELISA. n = 3. (L) Primary NPCs were induced with TBHP, and then treated with treated A1TP-EVs and A1TP-OE-EVs for 24 h. Cell lysates were immunoblotted with indicated antibodies. (M) Primary NPCs were induced with TBHP, and then treated with A1TP-EVs and A1TP-OE-EVs for 24 h, followed by immunofluorescent staining with anti-TOM20 (green) and anti-4-HNE (red) antibodies. n = 3. Scale bar, 50 μm. (N-O) Representative oxygen consumption traces of primary NPCs induced with TBHP and then treated with A1TP-HX-EVs, A1TP-KD-HX-EVs, or A1TP-OE-EVs for 24 h. Maximal respiration of NPCs were quantified. n = 3. All data are expressed as the mean ± SD. For E), I), M) and O), one‐way ANOVA with Tukey's multiple comparison tests were used for statistical analysis. For D), G) and K), two‐tailed unpaired Student's t‐tests were used for statistical analysis. ∗ P < 0.05. ∗∗ P < 0.01. ∗∗∗ P < 0.001. ns, not significant.

Techniques: Liquid Chromatography with Mass Spectroscopy, Inhibition, Derivative Assay, Enzyme-linked Immunosorbent Assay, shRNA, Knockdown, Staining, Comparison, Two Tailed Test

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anti 4 hydroxynonenal 4 hne antibody (R&D Systems)

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