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kukoamine b  (MedChemExpress)


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    Structured Review

    MedChemExpress kukoamine b
    TrxR2 prevented ferroptosis by suppressing the formation of lipid peroxidation. (A) Principal component analysis of indicated groups. (B,C) Volcano plots and KEGG analysis of differentially expressed genes (DEGs), as identified by RNA‐sequencing assay in HCMECs treated with HG/PA, with or without TrxR2 overexpression. (D) A heat map of ferroptosis genes in the indicated groups. (E–G) Lipidomic analysis of HCMECs following HG/PA treatment (E); the levels of all major PE species are summarized in a heatmap (F). PE molecular species (18:0/20:4) and (18:0/22:4) as well as hydroperoxy‐PE molecular species (18:0/20:4) and (18:0/22:4) were quantitatively assessed (G) ( n = 8 per group). (H) Representative immunofluorescence images and quantification of BODIPY C11 staining in the indicated groups ( n = 6 per group). (I,J) LDH released into the supernatant and the surviving fraction were quantitatively analyzed ( n = 6 per group). (K) Molecular docking analysis predicted that <t>Kukoamine</t> <t>B</t> forms six hydrogen bonds with TrxR2. (L) Representative immunofluorescence images of BODIPY C11 staining in HCMECs treated with HG/PA and/or Kuk B (10 µ m ) for 72 h ( n = 6 per group). (M) Multiple endothelial cell lines were treated with 10 µ m Kukoamine B (Kuk B) for 24 h, followed by exposure to RSL3 at indicated concentrations for 6 h. The relative cell viability is summarized in a heatmap ( n = 3 per group). Unpaired Student's t‐test was used for G. Two‐way ANOVA, followed by Tukey's post‐hoc multi‐comparison test, was used for H, I, and J. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate statistically significant differences. Kuk B, Kukoamine B; PCA, principal component analysis; PE, phosphatidylethanolamine.
    Kukoamine B, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n2393/Kukoamine+B/pmc13088291-211-13-19
    Average 94 stars, based on 1 article reviews
    kukoamine b - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy"

    Article Title: TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy

    Journal: Advanced Science

    doi: 10.1002/advs.202521997

    TrxR2 prevented ferroptosis by suppressing the formation of lipid peroxidation. (A) Principal component analysis of indicated groups. (B,C) Volcano plots and KEGG analysis of differentially expressed genes (DEGs), as identified by RNA‐sequencing assay in HCMECs treated with HG/PA, with or without TrxR2 overexpression. (D) A heat map of ferroptosis genes in the indicated groups. (E–G) Lipidomic analysis of HCMECs following HG/PA treatment (E); the levels of all major PE species are summarized in a heatmap (F). PE molecular species (18:0/20:4) and (18:0/22:4) as well as hydroperoxy‐PE molecular species (18:0/20:4) and (18:0/22:4) were quantitatively assessed (G) ( n = 8 per group). (H) Representative immunofluorescence images and quantification of BODIPY C11 staining in the indicated groups ( n = 6 per group). (I,J) LDH released into the supernatant and the surviving fraction were quantitatively analyzed ( n = 6 per group). (K) Molecular docking analysis predicted that Kukoamine B forms six hydrogen bonds with TrxR2. (L) Representative immunofluorescence images of BODIPY C11 staining in HCMECs treated with HG/PA and/or Kuk B (10 µ m ) for 72 h ( n = 6 per group). (M) Multiple endothelial cell lines were treated with 10 µ m Kukoamine B (Kuk B) for 24 h, followed by exposure to RSL3 at indicated concentrations for 6 h. The relative cell viability is summarized in a heatmap ( n = 3 per group). Unpaired Student's t‐test was used for G. Two‐way ANOVA, followed by Tukey's post‐hoc multi‐comparison test, was used for H, I, and J. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate statistically significant differences. Kuk B, Kukoamine B; PCA, principal component analysis; PE, phosphatidylethanolamine.
    Figure Legend Snippet: TrxR2 prevented ferroptosis by suppressing the formation of lipid peroxidation. (A) Principal component analysis of indicated groups. (B,C) Volcano plots and KEGG analysis of differentially expressed genes (DEGs), as identified by RNA‐sequencing assay in HCMECs treated with HG/PA, with or without TrxR2 overexpression. (D) A heat map of ferroptosis genes in the indicated groups. (E–G) Lipidomic analysis of HCMECs following HG/PA treatment (E); the levels of all major PE species are summarized in a heatmap (F). PE molecular species (18:0/20:4) and (18:0/22:4) as well as hydroperoxy‐PE molecular species (18:0/20:4) and (18:0/22:4) were quantitatively assessed (G) ( n = 8 per group). (H) Representative immunofluorescence images and quantification of BODIPY C11 staining in the indicated groups ( n = 6 per group). (I,J) LDH released into the supernatant and the surviving fraction were quantitatively analyzed ( n = 6 per group). (K) Molecular docking analysis predicted that Kukoamine B forms six hydrogen bonds with TrxR2. (L) Representative immunofluorescence images of BODIPY C11 staining in HCMECs treated with HG/PA and/or Kuk B (10 µ m ) for 72 h ( n = 6 per group). (M) Multiple endothelial cell lines were treated with 10 µ m Kukoamine B (Kuk B) for 24 h, followed by exposure to RSL3 at indicated concentrations for 6 h. The relative cell viability is summarized in a heatmap ( n = 3 per group). Unpaired Student's t‐test was used for G. Two‐way ANOVA, followed by Tukey's post‐hoc multi‐comparison test, was used for H, I, and J. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate statistically significant differences. Kuk B, Kukoamine B; PCA, principal component analysis; PE, phosphatidylethanolamine.

    Techniques Used: RNA Sequencing, Over Expression, Immunofluorescence, Staining, Comparison

    Related Articles

    Activity Assay:

    Article Title: TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy
    Article Snippet: To induce ferroptosis, the cells were treated with RSL3 (MCE, USA) at the indicated concentrations for 4–6 h. Cells were exposed to Alda‐1 (10 μ m ) for 24 h to enhance ALDH2 activity. .. To inhibit or stimulate TrxR2 activity, MitoCur‐1 (10 μ m , MCE), or Kukoamine B (10 μ m , MCE) was applied for the indicated durations. .. The SCP2 inducer 4‐hydroxytamoxifen (4OHT, 1 μM; Macklin, China) or the activity inhibitor ScpI2 (5 μ m ; Vitas‐M, Netherlands) was used to regulate SCP2 activity [ ].

    Article Title: TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy.
    Article Snippet: To induce ferroptosis, the cells were treated with RSL3 (MCE, USA) at the indicated concentrations for 4–6 h. Cells were exposed to Alda1 (10 μm ) for 24 h to enhance ALDH2 activity. .. To inhibit or stimulate TrxR2 activity, MitoCur-1 (10 μm , MCE), or Kukoamine B (10 μm , MCE) was applied for the indicated durations. .. The SCP2 inducer 4-hydroxytamoxifen (4OHT, 1 μM; Macklin, China) or the activity inhibitor ScpI2 (5 μm ; Vitas-M, Netherlands) was used to regulate SCP2 activity [ 50 ].



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    kukoamine b  (MedChemExpress)
    94
    MedChemExpress kukoamine b
    TrxR2 prevented ferroptosis by suppressing the formation of lipid peroxidation. (A) Principal component analysis of indicated groups. (B,C) Volcano plots and KEGG analysis of differentially expressed genes (DEGs), as identified by RNA‐sequencing assay in HCMECs treated with HG/PA, with or without TrxR2 overexpression. (D) A heat map of ferroptosis genes in the indicated groups. (E–G) Lipidomic analysis of HCMECs following HG/PA treatment (E); the levels of all major PE species are summarized in a heatmap (F). PE molecular species (18:0/20:4) and (18:0/22:4) as well as hydroperoxy‐PE molecular species (18:0/20:4) and (18:0/22:4) were quantitatively assessed (G) ( n = 8 per group). (H) Representative immunofluorescence images and quantification of BODIPY C11 staining in the indicated groups ( n = 6 per group). (I,J) LDH released into the supernatant and the surviving fraction were quantitatively analyzed ( n = 6 per group). (K) Molecular docking analysis predicted that <t>Kukoamine</t> <t>B</t> forms six hydrogen bonds with TrxR2. (L) Representative immunofluorescence images of BODIPY C11 staining in HCMECs treated with HG/PA and/or Kuk B (10 µ m ) for 72 h ( n = 6 per group). (M) Multiple endothelial cell lines were treated with 10 µ m Kukoamine B (Kuk B) for 24 h, followed by exposure to RSL3 at indicated concentrations for 6 h. The relative cell viability is summarized in a heatmap ( n = 3 per group). Unpaired Student's t‐test was used for G. Two‐way ANOVA, followed by Tukey's post‐hoc multi‐comparison test, was used for H, I, and J. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate statistically significant differences. Kuk B, Kukoamine B; PCA, principal component analysis; PE, phosphatidylethanolamine.
    Kukoamine B, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n2393/Kukoamine+B/pmc13088291-211-13-19
    Average 94 stars, based on 1 article reviews
    kukoamine b - by Bioz Stars, 2026-10
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    TrxR2 prevented ferroptosis by suppressing the formation of lipid peroxidation. (A) Principal component analysis of indicated groups. (B,C) Volcano plots and KEGG analysis of differentially expressed genes (DEGs), as identified by RNA‐sequencing assay in HCMECs treated with HG/PA, with or without TrxR2 overexpression. (D) A heat map of ferroptosis genes in the indicated groups. (E–G) Lipidomic analysis of HCMECs following HG/PA treatment (E); the levels of all major PE species are summarized in a heatmap (F). PE molecular species (18:0/20:4) and (18:0/22:4) as well as hydroperoxy‐PE molecular species (18:0/20:4) and (18:0/22:4) were quantitatively assessed (G) ( n = 8 per group). (H) Representative immunofluorescence images and quantification of BODIPY C11 staining in the indicated groups ( n = 6 per group). (I,J) LDH released into the supernatant and the surviving fraction were quantitatively analyzed ( n = 6 per group). (K) Molecular docking analysis predicted that Kukoamine B forms six hydrogen bonds with TrxR2. (L) Representative immunofluorescence images of BODIPY C11 staining in HCMECs treated with HG/PA and/or Kuk B (10 µ m ) for 72 h ( n = 6 per group). (M) Multiple endothelial cell lines were treated with 10 µ m Kukoamine B (Kuk B) for 24 h, followed by exposure to RSL3 at indicated concentrations for 6 h. The relative cell viability is summarized in a heatmap ( n = 3 per group). Unpaired Student's t‐test was used for G. Two‐way ANOVA, followed by Tukey's post‐hoc multi‐comparison test, was used for H, I, and J. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate statistically significant differences. Kuk B, Kukoamine B; PCA, principal component analysis; PE, phosphatidylethanolamine.

    Journal: Advanced Science

    Article Title: TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy

    doi: 10.1002/advs.202521997

    Figure Lengend Snippet: TrxR2 prevented ferroptosis by suppressing the formation of lipid peroxidation. (A) Principal component analysis of indicated groups. (B,C) Volcano plots and KEGG analysis of differentially expressed genes (DEGs), as identified by RNA‐sequencing assay in HCMECs treated with HG/PA, with or without TrxR2 overexpression. (D) A heat map of ferroptosis genes in the indicated groups. (E–G) Lipidomic analysis of HCMECs following HG/PA treatment (E); the levels of all major PE species are summarized in a heatmap (F). PE molecular species (18:0/20:4) and (18:0/22:4) as well as hydroperoxy‐PE molecular species (18:0/20:4) and (18:0/22:4) were quantitatively assessed (G) ( n = 8 per group). (H) Representative immunofluorescence images and quantification of BODIPY C11 staining in the indicated groups ( n = 6 per group). (I,J) LDH released into the supernatant and the surviving fraction were quantitatively analyzed ( n = 6 per group). (K) Molecular docking analysis predicted that Kukoamine B forms six hydrogen bonds with TrxR2. (L) Representative immunofluorescence images of BODIPY C11 staining in HCMECs treated with HG/PA and/or Kuk B (10 µ m ) for 72 h ( n = 6 per group). (M) Multiple endothelial cell lines were treated with 10 µ m Kukoamine B (Kuk B) for 24 h, followed by exposure to RSL3 at indicated concentrations for 6 h. The relative cell viability is summarized in a heatmap ( n = 3 per group). Unpaired Student's t‐test was used for G. Two‐way ANOVA, followed by Tukey's post‐hoc multi‐comparison test, was used for H, I, and J. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate statistically significant differences. Kuk B, Kukoamine B; PCA, principal component analysis; PE, phosphatidylethanolamine.

    Article Snippet: To inhibit or stimulate TrxR2 activity, MitoCur‐1 (10 μ m , MCE), or Kukoamine B (10 μ m , MCE) was applied for the indicated durations.

    Techniques: RNA Sequencing, Over Expression, Immunofluorescence, Staining, Comparison