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lipid peroxide content detection kit  (Beijing Solarbio Science)


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    Beijing Solarbio Science lipid peroxide content detection kit
    3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; <t>MDA:</t> <t>Malondialdehyde;</t> LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.
    Lipid Peroxide Content Detection Kit, supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lipid peroxide content detection kit/product/Beijing Solarbio Science
    Average 90 stars, based on 1 article reviews
    lipid peroxide content detection kit - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate"

    Article Title: Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate

    Journal: Gut Microbes

    doi: 10.1080/19490976.2025.2486515

    3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.
    Figure Legend Snippet: 3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.

    Techniques Used: Expressing, Binding Assay, Recombinant, Staining, Western Blot

    3-HB inhibits ferroptosis in mice by activating the PI3K/AKT/mTOR/LPIN1 pathway. (a) GSEA-kegg analysis. (b) Relative mRNA levels of Acsl4, Gpx4, SLC7a11, Fth1 and hmox-1 genes, n = 5–6. (c, d) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (e-g) MDA, LPO and Fe 2+ content in liver tissue, n = 6. (h, i) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (j) Relative ACSL4 mRNA expression level, n = 6–8. (k-m) MDA, LPO and Fe 2+ content in liver tissue from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6. (n) ACSL4 immunofluorescence of liver tissue from WT and Lpin1KO mice, scale: 100 μm, n = 6. (o) Quantitative analysis of ACSL4 immunofluorescence intensity, n = 6. (p) Relative ACSL4 mRNA expression level, n = 6–8. (q-s) MDA, LPO and Fe 2+ content in liver tissue from WT and Lpin1KO mice, n = 6. The results are expressed as the median and quartile. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test)(B-G) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.
    Figure Legend Snippet: 3-HB inhibits ferroptosis in mice by activating the PI3K/AKT/mTOR/LPIN1 pathway. (a) GSEA-kegg analysis. (b) Relative mRNA levels of Acsl4, Gpx4, SLC7a11, Fth1 and hmox-1 genes, n = 5–6. (c, d) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (e-g) MDA, LPO and Fe 2+ content in liver tissue, n = 6. (h, i) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (j) Relative ACSL4 mRNA expression level, n = 6–8. (k-m) MDA, LPO and Fe 2+ content in liver tissue from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6. (n) ACSL4 immunofluorescence of liver tissue from WT and Lpin1KO mice, scale: 100 μm, n = 6. (o) Quantitative analysis of ACSL4 immunofluorescence intensity, n = 6. (p) Relative ACSL4 mRNA expression level, n = 6–8. (q-s) MDA, LPO and Fe 2+ content in liver tissue from WT and Lpin1KO mice, n = 6. The results are expressed as the median and quartile. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test)(B-G) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.

    Techniques Used: Immunofluorescence, Expressing

    3-HB alleviates AML12 cell injury by activating the PI3K/AKT/mTOR/LPIN1 pathway to inhibit ferroptosis. (a) AML12 cell viability was detected by CCk8, n = 6. (b) LDH content in AML12 cell supernatant, n = 6. (c-f) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells, n = 4. (g) AML12 cell viability by CCk8, n = 6. (h) LDH content in AML12 cell supernatant, n = 6. (i-k) the protein expression levels of p-akt, PI3K, p-mTOR, LPIN1 and ACSL4 in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235 ( n = 3). (l-o) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235, n = 4. (p) LPIN1 protein expression level, n = 4. (q) The protein expression levels of LPIN1 and ACSL4 in the AML12 cells ( n = 3). (r) AML12 cell viability by CCk8, n = 6. (s) LDH content in AML12 cell supernatant, n = 6. (t-w) MDA, LPO, TGSH and Fe 2+ content in AML12 cells transfected with Ctrl shRNA and Lpin1 shRNA, n = 4. The results are expressed as the mean ± SEM. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test) (A-F) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.
    Figure Legend Snippet: 3-HB alleviates AML12 cell injury by activating the PI3K/AKT/mTOR/LPIN1 pathway to inhibit ferroptosis. (a) AML12 cell viability was detected by CCk8, n = 6. (b) LDH content in AML12 cell supernatant, n = 6. (c-f) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells, n = 4. (g) AML12 cell viability by CCk8, n = 6. (h) LDH content in AML12 cell supernatant, n = 6. (i-k) the protein expression levels of p-akt, PI3K, p-mTOR, LPIN1 and ACSL4 in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235 ( n = 3). (l-o) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235, n = 4. (p) LPIN1 protein expression level, n = 4. (q) The protein expression levels of LPIN1 and ACSL4 in the AML12 cells ( n = 3). (r) AML12 cell viability by CCk8, n = 6. (s) LDH content in AML12 cell supernatant, n = 6. (t-w) MDA, LPO, TGSH and Fe 2+ content in AML12 cells transfected with Ctrl shRNA and Lpin1 shRNA, n = 4. The results are expressed as the mean ± SEM. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test) (A-F) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.

    Techniques Used: Expressing, Transfection, shRNA


    Figure Legend Snippet:

    Techniques Used: Virus, Ligation, Transplantation Assay, Recombinant



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    3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; <t>MDA:</t> <t>Malondialdehyde;</t> LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.
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    3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; <t>MDA:</t> <t>Malondialdehyde;</t> LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.
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    Image Search Results


    3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.

    Journal: Gut Microbes

    Article Title: Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate

    doi: 10.1080/19490976.2025.2486515

    Figure Lengend Snippet: 3-HB activates the PI3K/AKT/mTOR/LPIN1 signaling pathway to protect against septic liver injury. (a) Principal component analysis, n = 5–6. (b) Volcanic plot of differential genes between CLP and CLP + 3-HB groups. (c) Differential gene heat map of CLP and CLP + 3-HB groups. (d) KEGG pathway analysis. (e, f) protein expression levels of AKT, p-akt, PI3K, mTOR, p-mTOR and LPIN1 in liver tissue were detected by WB ( n = 3). (g) Molecular docking analysis of 3-HB with the PI3K protein (PDB: 1E8Y). (h) SPR analysis of 3-HB (40, 80, 100 and 400 μM) binding to the recombinant human (rh) protein of rhPIK3R3 (Sf9, his, GST). (i) HE staining of liver tissues from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, scale: 100 μm, n = 6. (j) Liver histopathological damage scores, n = 6. (k, l) ALT and AST content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (m) LPS content in serum from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6–8. (n, o) the protein expression levels of p-akt, PI3K, p-mTOR and LPIN1 in liver tissue ( n = 3). (p) Relative Lpin1 mRNA expression level, n = 6. (q) LPS content in serum from WT and Lpin1KO mice, n = 6. (r, s) HE staining and liver histopathological damage scores, scale: 100 μm, n = 6. (t, u) ALT and AST content in serum from WT and Lpin1KO mice, n = 6–8. The results are expressed as the mean ± SEM (F, O) and the median and quartile. * p < 0.05, ** p < 0.01, *** p < 0.001 by one-way ANOVA (Tukey’s test)(f) and two-way ANOVA (Tukey’s test)(K-U). WB: Western blot; 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; PCA: Principal component Analysis; SEM, standard error of mean; rh: recombinant human.

    Article Snippet: The levels of MDA, LPO, and Fe 2+ in liver tissue and AML12 cells were assessed using the malondialdehyde (MDA) content detection kit, lipid peroxide (LPO) content detection kit, and iron content detection kit (Solarbio, Beijing, China).

    Techniques: Expressing, Binding Assay, Recombinant, Staining, Western Blot

    3-HB inhibits ferroptosis in mice by activating the PI3K/AKT/mTOR/LPIN1 pathway. (a) GSEA-kegg analysis. (b) Relative mRNA levels of Acsl4, Gpx4, SLC7a11, Fth1 and hmox-1 genes, n = 5–6. (c, d) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (e-g) MDA, LPO and Fe 2+ content in liver tissue, n = 6. (h, i) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (j) Relative ACSL4 mRNA expression level, n = 6–8. (k-m) MDA, LPO and Fe 2+ content in liver tissue from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6. (n) ACSL4 immunofluorescence of liver tissue from WT and Lpin1KO mice, scale: 100 μm, n = 6. (o) Quantitative analysis of ACSL4 immunofluorescence intensity, n = 6. (p) Relative ACSL4 mRNA expression level, n = 6–8. (q-s) MDA, LPO and Fe 2+ content in liver tissue from WT and Lpin1KO mice, n = 6. The results are expressed as the median and quartile. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test)(B-G) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.

    Journal: Gut Microbes

    Article Title: Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate

    doi: 10.1080/19490976.2025.2486515

    Figure Lengend Snippet: 3-HB inhibits ferroptosis in mice by activating the PI3K/AKT/mTOR/LPIN1 pathway. (a) GSEA-kegg analysis. (b) Relative mRNA levels of Acsl4, Gpx4, SLC7a11, Fth1 and hmox-1 genes, n = 5–6. (c, d) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (e-g) MDA, LPO and Fe 2+ content in liver tissue, n = 6. (h, i) ACSL4 immunofluorescence and quantification in liver tissues, scale: 100 μm, n = 6. (j) Relative ACSL4 mRNA expression level, n = 6–8. (k-m) MDA, LPO and Fe 2+ content in liver tissue from mice in the CLP, CLP+NVP-BEZ235, CLP + 3-HB, and CLP + 3-HB+NVP-BEZ235 groups, n = 6. (n) ACSL4 immunofluorescence of liver tissue from WT and Lpin1KO mice, scale: 100 μm, n = 6. (o) Quantitative analysis of ACSL4 immunofluorescence intensity, n = 6. (p) Relative ACSL4 mRNA expression level, n = 6–8. (q-s) MDA, LPO and Fe 2+ content in liver tissue from WT and Lpin1KO mice, n = 6. The results are expressed as the median and quartile. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test)(B-G) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; ALT: alanine Aminotransferase; AST: aspartate aminotransferase; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.

    Article Snippet: The levels of MDA, LPO, and Fe 2+ in liver tissue and AML12 cells were assessed using the malondialdehyde (MDA) content detection kit, lipid peroxide (LPO) content detection kit, and iron content detection kit (Solarbio, Beijing, China).

    Techniques: Immunofluorescence, Expressing

    3-HB alleviates AML12 cell injury by activating the PI3K/AKT/mTOR/LPIN1 pathway to inhibit ferroptosis. (a) AML12 cell viability was detected by CCk8, n = 6. (b) LDH content in AML12 cell supernatant, n = 6. (c-f) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells, n = 4. (g) AML12 cell viability by CCk8, n = 6. (h) LDH content in AML12 cell supernatant, n = 6. (i-k) the protein expression levels of p-akt, PI3K, p-mTOR, LPIN1 and ACSL4 in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235 ( n = 3). (l-o) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235, n = 4. (p) LPIN1 protein expression level, n = 4. (q) The protein expression levels of LPIN1 and ACSL4 in the AML12 cells ( n = 3). (r) AML12 cell viability by CCk8, n = 6. (s) LDH content in AML12 cell supernatant, n = 6. (t-w) MDA, LPO, TGSH and Fe 2+ content in AML12 cells transfected with Ctrl shRNA and Lpin1 shRNA, n = 4. The results are expressed as the mean ± SEM. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test) (A-F) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.

    Journal: Gut Microbes

    Article Title: Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate

    doi: 10.1080/19490976.2025.2486515

    Figure Lengend Snippet: 3-HB alleviates AML12 cell injury by activating the PI3K/AKT/mTOR/LPIN1 pathway to inhibit ferroptosis. (a) AML12 cell viability was detected by CCk8, n = 6. (b) LDH content in AML12 cell supernatant, n = 6. (c-f) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells, n = 4. (g) AML12 cell viability by CCk8, n = 6. (h) LDH content in AML12 cell supernatant, n = 6. (i-k) the protein expression levels of p-akt, PI3K, p-mTOR, LPIN1 and ACSL4 in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235 ( n = 3). (l-o) MDA, LPO, TGSH and Fe 2+ content in the AML12 cells treated with LPS, LPS+NVP-BEZ235, LPS + 3-HB, and LPS + 3-HB+NVP-BEZ235, n = 4. (p) LPIN1 protein expression level, n = 4. (q) The protein expression levels of LPIN1 and ACSL4 in the AML12 cells ( n = 3). (r) AML12 cell viability by CCk8, n = 6. (s) LDH content in AML12 cell supernatant, n = 6. (t-w) MDA, LPO, TGSH and Fe 2+ content in AML12 cells transfected with Ctrl shRNA and Lpin1 shRNA, n = 4. The results are expressed as the mean ± SEM. * p < 0.05,** p < 0.01,*** p < 0.001 by one-way ANOVA (Tukey’s test) (A-F) and two-way ANOVA (Tukey’s test). 3-HB: 3-hydroxybutyric acid; MDA: Malondialdehyde; LPO: lipid Peroxidation; SEM, standard error of mean.

    Article Snippet: The levels of MDA, LPO, and Fe 2+ in liver tissue and AML12 cells were assessed using the malondialdehyde (MDA) content detection kit, lipid peroxide (LPO) content detection kit, and iron content detection kit (Solarbio, Beijing, China).

    Techniques: Expressing, Transfection, shRNA

    Journal: Gut Microbes

    Article Title: Time-restricted feeding protects against septic liver injury by reshaping gut microbiota and metabolite 3-hydroxybutyrate

    doi: 10.1080/19490976.2025.2486515

    Figure Lengend Snippet:

    Article Snippet: The levels of MDA, LPO, and Fe 2+ in liver tissue and AML12 cells were assessed using the malondialdehyde (MDA) content detection kit, lipid peroxide (LPO) content detection kit, and iron content detection kit (Solarbio, Beijing, China).

    Techniques: Virus, Ligation, Transplantation Assay, Recombinant