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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 364 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+4+hne/4-Hydroxynonenal+Antibody/pm41986303-232-21-25
Average 96 stars, based on 364 article reviews

anti 4 hydroxynonenal 4 hne antibody - by Bioz Stars, 2026-09

96/100 stars

Images

Staining:

Article Title: Photocuring CsA and bFGF-embedded hemostatic hydrogel promotes recovery from TBI by mitigating ferroptosis and neuroinflammation
Article Snippet: .. 20 μm sections were cut and stained with primary anti-HO-1 (1:500; sc-136960, Santa Cruz, USA), anti-4-HNE (1:500; MAB3249, R&D Systems, USA) overnight at 4°C, followed by incubation with HRP-conjugated goat anti-mouse/rabbit IgG H&L (PV-9000, ZSGB Biotechnology. ..

Incubation:

Article Title: H3K14 lactylation exacerbates neuronal ferroptosis by inhibiting calcium efflux following intracerebral hemorrhagic stroke
Article Snippet: EDGE, VILBER) using the Immobilon Wester chemilum HRP substrates (WBKLS0500, Millipore). .. Western blot was incubated with the following antibodies: anti-Histone H3 (mono methyl K9) antibody (1:10,000, ab9045, Abcam), anti-Histone H3 (di methyl K9) antibody (1:10,000, ab1220, Abcam), anti-Histone H3 (tri methyl K9) antibody (1:10,000, ab8898, Abcam), anti-Histone H3 (mono methyl K27) antibody (1:10,000, ab194688, Abcam), anti-Histone H3 (di methyl K27) antibody (1:10,000, ab24684, Abcam), anti-Histone H3 (tri methyl K27) antibody (1:10,000, ab192985, Abcam), anti-acetyl Lysine antibody (1:1000, ab80178, Abcam), anti-Histone H3 (mono methyl K4) antibody (1:1000, GTX54100, GeneTex), anti-Histone H3 (di methyl K4) antibody (1:1000, ab32356, Abcam), anti-Histone H3 (tri methyl K4) antibody (1:1000, ab8580, Abcam), Anti-L-Lactyl Lysine rabbit mAb antibody (1:1000, PTM-1401RM, PTM BIO), anti-L-Lactyl-Histone H3 (Lys14) rabbit mAb (1:1000, PTM-1414RM, PTM BIO), anti-L-Lactyl-Histone H4 (Lys8) rabbit mAb (1:1000, PTM-1415RM, PTM BIO), anti-L-Lactyl-Histone H4 (Lys5) rabbit mAb (1:1000, PTM-1407RM, PTM BIO), anti-H3 antibody (1:2000, ab10799, Abcam), anti-H4 antibody (1:2000, PTM-1009RM, PTM BIO), anti-spectrin (1:500; BML-FG6090; Enzo), anti-rabbit IgG, HRP-linked antibody (1:1000, 7071S, CST, USA), anti-mouse IgG, HRP-linked antibody (1:1000, 7076S, CST), anti-4-HNE (1:1000, MAB3249, R&D system). ..

Article Title: H3K14 lactylation exacerbates neuronal ferroptosis by inhibiting calcium efflux following intracerebral hemorrhagic stroke.
Article Snippet: EDGE, VILBER) using the Immobilon Wester chemilum HRP substrates (WBKLS0500, Millipore). .. Western blot was incubated with the following antibodies: anti-Histone H3 (mono methyl K9) antibody (1:10,000, ab9045, Abcam), anti-Histone H3 (di methyl K9) antibody (1:10,000, ab1220, Abcam), anti-Histone H3 (tri methyl K9) antibody (1:10,000, ab8898, Abcam), anti-Histone H3 (mono methyl K27) antibody (1:10,000, ab194688, Abcam), anti-Histone H3 (di methyl K27) antibody (1:10,000, ab24684, Abcam), anti-Histone H3 (tri methyl K27) antibody (1:10,000, ab192985, Abcam), anti-acetyl Lysine antibody (1:1000, ab80178, Abcam), anti-Histone H3 (mono methyl K4) antibody (1:1000, GTX54100, GeneTex), anti-Histone H3 (di methyl K4) antibody (1:1000, ab32356, Abcam), anti-Histone H3 (tri methyl K4) antibody (1:1000, ab8580, Abcam), Anti-L-Lactyl Lysine rabbit mAb antibody (1:1000, PTM-1401RM, PTM BIO), anti-L-LactylHistone H3 (Lys14) rabbit mAb (1:1000, PTM-1414RM, PTM BIO), anti-LLactyl-Histone H4 (Lys8) rabbit mAb (1:1000, PTM-1415RM, PTM BIO), anti-L-Lactyl-Histone H4 (Lys5) rabbit mAb (1:1000, PTM-1407RM, PTM BIO), anti-H3 antibody (1:2000, ab10799, Abcam), anti-H4 antibody (1:2000, PTM-1009RM, PTM BIO), anti-spectrin (1:500; BML-FG6090; Enzo), anti-rabbit IgG, HRP-linked antibody (1:1000, 7071S, CST, USA), anti-mouse IgG, HRP-linked antibody (1:1000, 7076S, CST), anti-4-HNE (1:1000, MAB3249, R&D system). ..

Article Title: Placental Ferroptosis and Impaired Fetal Growth in Symptomatic and Asymptomatic SARS-CoV-2 Infections
Article Snippet: .. Sections were then182 incubated with rabbit polyclonal anti-ferritin (1:1500 dilution, Invitrogen, PA5-120011)183 or anti-4-HNE (1:1000 dilution, R&D Systems, MAB3249) antibodies for 30 minutes184 at room temperature. ..

Flow Cytometry:

Article Title: Epithelial HO-1 regulates iron availability and promotes colonic tumorigenesis in a context-dependent manner.
Article Snippet: Dead cells were stained and excluded using BioLegend 7AAD viability staining solution or Zombie AquaTM dye prior to flow cytometry or FACS. .. Anti-4-HNE (R&D Systems [MAB3249]) was used with an AF647 secondary antibody (Invitrogen) to detect lipid peroxidation via flow cytometry, which was validated using H2O2 as a positive control. .. Other anti-mouse antibodies were purchased from BioLegend or Thermo Fisher Scientific: CD45 (30-F11); EpCAM (G8.8).

Article Title: Epithelial HO-1 regulates iron availability and promotes colonic tumorigenesis in a context-dependent manner
Article Snippet: Dead cells were stained and excluded using BioLegend 7AAD viability staining solution or Zombie Aqua dye prior to flow cytometry or FACS. .. Anti-4-HNE (R&D Systems, MAB3249) was used with an AF647 secondary antibody (Invitrogen) to detect lipid peroxidation via flow cytometry, which was validated using H 2 O 2 as a positive control. .. Other anti-mouse antibodies were purchased from BioLegend or Thermo Fisher Scientific: CD45 (30-F11) and EpCAM (G8.8).

Positive Control:

Immunohistochemistry:

Article Title: The cyclin-dependent kinase inhibitor p27 facilitates chemosensitivity by promoting ferroptosis in epithelial ovarian cancer
Article Snippet: Erastin (S7242), ferrostatin-1 (S7243), and Skp2 inhibitor C1 (SKPin C1) (S8652) were purchased from Selleck Chemical. .. The primary antibodies used for IHC included anti-p27 (Proteintech; 25614-1-AP; 1:50 dilution), anti-Ki67 (Proteintech; 27309-1-AP; 1:3000 dilution), anti-4-HNE (R&D Systems; MAB3249; 1:200 dilution), anti-CYBB (Proteintech; 19013-1-AP; 1:100 dilution), and anti- Cleaved Caspase-3 (CST; 9661; 1:100 dilution). .. The primary antibodies used for Western blot included anti-p27 (Proteintech; 25614-1-AP; 1:1000 dilution), anti-CYBB (Proteintech; 19013-1-AP; 1:1000 dilution), anti-Skp2 (Proteintech; 15010-1-AP; 1:1000 dilution), anti-β-actin (ABclonal; AC026; 1:10,000 dilution), and anti-Vinculin (Proteintech; 26520-1-AP; 1:10,000 dilution).

Article Title: The cyclin-dependent kinase inhibitor p27 facilitates chemosensitivity by promoting ferroptosis in epithelial ovarian cancer.
Article Snippet: Erastin 398 (S7242), ferrostatin-1 (S7243), and Skp2 inhibitor C1 (SKPin C1) (S8652) were purchased 399 from Selleck Chemical (USA). .. 400 The primary antibodies used for IHC included anti-p27 (Proteintech; 25614-1-AP; 1:50 401 dilution), anti-Ki67 (Proteintech; 27309-1-AP; 1:3000 dilution), anti-4-HNE (R&D Systems; 402 MAB3249; 1:200 dilution), anti-CYBB (Proteintech; 19013-1-AP; 1:100 dilution), and anti- 403 Cleaved Caspase-3 (CST; 9661; 1:100 dilution). .. The primary antibodies used for Western blot 404 included anti-p27 (Proteintech; 25614-1-AP; 1:1000 dilution), anti-CYBB (Proteintech; 19013-405 1-AP; 1:1000 dilution), anti-Skp2 (Proteintech; 15010-1-AP; 1:1000 dilution), anti-β-actin 406 (ABclonal; AC026; 1:10000 dilution), and anti-Vinculin (Proteintech; 26520-1-AP; 1:10000 407 dilution).

Western Blot:

Image Search Results

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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Staining:

Incubation:

Flow Cytometry:

Positive Control:

Immunohistochemistry:

Western Blot:

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