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hep g2  (ATCC)


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    ATCC hep g2
    Hep G2, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 29584 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hepatocellular+carcinoma+cells/custom%40hb-8065%4010%2E1016%2Fj%2Esajb%2E2026%2E07%2E014?v=ATCC
    Average 99 stars, based on 29584 article reviews
    hep g2 - by Bioz Stars, 2026-08
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    hep g2  (ATCC)
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    Procell Inc exposure 151 human hepatocellular carcinoma cell line g2
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    Procell Inc hepg2 human hepatocellular carcinoma cells
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    ATCC hepg2 human hepatocellular carcinoma cell line
    Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced <t>HepG2</t> cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
    Hepg2 Human Hepatocellular Carcinoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC hepg2 human hepatocellular carcinoma cells
    Knockdown of L-FABP mitigated F-53B-induced damage in <t>HepG2</t> cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.
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    ATCC human hepatocellular carcinoma hepg2 cells
    Knockdown of L-FABP mitigated F-53B-induced damage in <t>HepG2</t> cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.
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    ATCC human hepatocellular carcinoma cells
    Knockdown of L-FABP mitigated F-53B-induced damage in <t>HepG2</t> cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.
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    Korean Cell Line Bank hepg2 human liver hepatocellular carcinoma cells
    Knockdown of L-FABP mitigated F-53B-induced damage in <t>HepG2</t> cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.
    Hepg2 Human Liver Hepatocellular Carcinoma Cells, supplied by Korean Cell Line Bank, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hepatocellular+carcinoma+cells/pm42072103-86-0-10?v=Korean+Cell+Line+Bank
    Average 86 stars, based on 1 article reviews
    hepg2 human liver hepatocellular carcinoma cells - by Bioz Stars, 2026-08
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    Interlab Inc human hepatocellular carcinoma cells
    Knockdown of L-FABP mitigated F-53B-induced damage in <t>HepG2</t> cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.
    Human Hepatocellular Carcinoma Cells, supplied by Interlab Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hepatocellular+carcinoma+cells/pm42072155-94-0-9?v=Interlab+Inc
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    human hepatocellular carcinoma cells - by Bioz Stars, 2026-08
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    ATCC human hepg2 hepatocellular carcinoma cells
    Mechanistic evaluation of combination treatment with the GLP-1R antagonist Exendin (9–39) on metabolic markers. Metabolic markers, including GLP-1R, AMPK, SIRT1, and resistin, were quantified in <t>HepG2</t> cells, while SIRT1 and UCP-1 levels was evaluated in 3T3-L1 adipocytes. Specifically, in ( A ) GLP-1R levels; in ( B ) AMPK levels; in ( C ) SIRT1 levels (HepG2 cells); in ( D ) Resistin levels; in ( E ) UCP-1 levels; in ( F ) SIRT1 levels (3T3-L1 cells). The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) from 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. * p < 0.05 vs. control; φ p < 0.05 vs. PA.
    Human Hepg2 Hepatocellular Carcinoma Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+hepatocellular+carcinoma+cells/pmc13164810-125-0-5?v=ATCC
    Average 99 stars, based on 1 article reviews
    human hepg2 hepatocellular carcinoma cells - by Bioz Stars, 2026-08
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    Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced HepG2 cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced HepG2 cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Control

    Sangyod rice extract inhibited apoptosis in OA-induced HepG2 cells by suppressing the Bax and caspase-3 pathway. (A) Representative images of nuclei stained with Hoechst 33342. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of apoptotic cells after treatment with Sangyod rice extract in OA-induced HepG2 cells. (C) Western blot analysis of Bax, Bcl-2, procaspase-3, and cleaved caspase-3. (D) Relative expression of Bax and Bcl-2. (E) Relative expression of procaspase 3, and cleaved caspase 3. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 compared to the control group, and #p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract inhibited apoptosis in OA-induced HepG2 cells by suppressing the Bax and caspase-3 pathway. (A) Representative images of nuclei stained with Hoechst 33342. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of apoptotic cells after treatment with Sangyod rice extract in OA-induced HepG2 cells. (C) Western blot analysis of Bax, Bcl-2, procaspase-3, and cleaved caspase-3. (D) Relative expression of Bax and Bcl-2. (E) Relative expression of procaspase 3, and cleaved caspase 3. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 compared to the control group, and #p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Staining, Western Blot, Expressing, Control

    Sangyod rice extract attenuated inflammation in OA-induced HepG2 cells through inhibition of the NF-κB pathway. (A) TNF-α gene, (B) IL-1β gene, (C) IL-6 gene, (D) IL-10 gene. (E) Western blot analysis of NF-κB. (F) Relative expression of NF-κB protein. Results are presented as the mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract attenuated inflammation in OA-induced HepG2 cells through inhibition of the NF-κB pathway. (A) TNF-α gene, (B) IL-1β gene, (C) IL-6 gene, (D) IL-10 gene. (E) Western blot analysis of NF-κB. (F) Relative expression of NF-κB protein. Results are presented as the mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Inhibition, Western Blot, Expressing, Control

    Sangyod rice extract reduced lipid accumulation in OA-induced HepG2 cells. (A) Oil Red O staining was conducted on HepG2 cells, with red fat droplets indicating lipid accumulation. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of lipid accumulation post Oil Red O extraction. (C) Levels of TG were measured using an assay kit. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract reduced lipid accumulation in OA-induced HepG2 cells. (A) Oil Red O staining was conducted on HepG2 cells, with red fat droplets indicating lipid accumulation. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of lipid accumulation post Oil Red O extraction. (C) Levels of TG were measured using an assay kit. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Staining, Extraction, Control

    Effect of Sangyod rice extract on lipid metabolism in OA-induced HepG2 cells. (A) SREBP-1c gene (B) ACC gene, (C) FASN gene (D) CPT-1 A gene, (E) SCD1 gene, (F) MTTP gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Effect of Sangyod rice extract on lipid metabolism in OA-induced HepG2 cells. (A) SREBP-1c gene (B) ACC gene, (C) FASN gene (D) CPT-1 A gene, (E) SCD1 gene, (F) MTTP gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Control

    Effect of Sangyod rice extract on the expression of LPL-1, LPL-2, PGC-1α and PPARα in OA-induced HepG2 cells. (A) LPL-1 gene (B) LPL-2 gene, (C) PPARα gene (D) PGC-1α gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Effect of Sangyod rice extract on the expression of LPL-1, LPL-2, PGC-1α and PPARα in OA-induced HepG2 cells. (A) LPL-1 gene (B) LPL-2 gene, (C) PPARα gene (D) PGC-1α gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Expressing, Control

    Sangyod rice extract regulates lipid metabolism through the Akt and MAPK signaling pathways. (A) Western blot analysis of Akt, ERK1/2 amd p38 MAPK, (B) Relative expression of pERK/ERK protein, (C) Relative expression of p-p38/p38 protein, (D) Relative expression of pAkt/Akt protein. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract regulates lipid metabolism through the Akt and MAPK signaling pathways. (A) Western blot analysis of Akt, ERK1/2 amd p38 MAPK, (B) Relative expression of pERK/ERK protein, (C) Relative expression of p-p38/p38 protein, (D) Relative expression of pAkt/Akt protein. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Protein-Protein interactions, Western Blot, Expressing, Control

    Knockdown of L-FABP mitigated F-53B-induced damage in HepG2 cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.

    Journal: iScience

    Article Title: F-53B exposure accelerates progression from preexisting fatty liver to non-alcoholic steatohepatitis and hepatic fibrosis

    doi: 10.1016/j.isci.2026.115675

    Figure Lengend Snippet: Knockdown of L-FABP mitigated F-53B-induced damage in HepG2 cells (A) Liver-type fatty acid-binding protein (L-FABP) knockdown was confirmed by immunoblot analysis using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as the loading control ( n = 6). (B) Calculated L-FABP/GAPDH ratio ( n = 6) based on the immunoblot results shown in (A). (C) Effects of different treatments on TG content in HepG2 cells ( n = 5). (D) Fold change of TG content in NC + F-53B/NC and L-FABP KD + F-53B/L-FABP KD groups ( n = 5). (E) Interleukin-6 (IL-6) expression in HepG2 cells following different treatments. (F) Relative IL-6 expression (IL-6/GAPDH) ( n = 6). (G) Fold change of IL-6 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). (H) Transforming growth factor β1 (TGF-β1) expression in HepG2 cells following different treatments. (I) Relative TGF-β1 expression (TGF-β1/GAPDH) ( n = 6). (J) Fold change of TGF-β1 (relative to respective control) in NC vs. L-FABP KD groups with F-53B treatment ( n = 6). NC, negative control siRNA group. NC + F-53B, NC with 5 mg/L F-53B group. L-FABP KD, L-FABP-knockdown group. L-FABP KD + F-53B, L-FABP KD with 5 mg/L F-53B group. Data are presented as mean ± SEM. The significance of differences between two groups was determined using the Mann-Whitney U test, and is indicated by hash symbols: # p < 0.05, ## p < 0.01.

    Article Snippet: HepG2 human hepatocellular carcinoma cells (ATCC, HB-8065) were maintained in a humidified incubator at 37 °C with 5% CO 2 .

    Techniques: Knockdown, Binding Assay, Western Blot, Control, Expressing, Negative Control, MANN-WHITNEY

    Mechanistic evaluation of combination treatment with the GLP-1R antagonist Exendin (9–39) on metabolic markers. Metabolic markers, including GLP-1R, AMPK, SIRT1, and resistin, were quantified in HepG2 cells, while SIRT1 and UCP-1 levels was evaluated in 3T3-L1 adipocytes. Specifically, in ( A ) GLP-1R levels; in ( B ) AMPK levels; in ( C ) SIRT1 levels (HepG2 cells); in ( D ) Resistin levels; in ( E ) UCP-1 levels; in ( F ) SIRT1 levels (3T3-L1 cells). The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) from 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. * p < 0.05 vs. control; φ p < 0.05 vs. PA.

    Journal: Nutrients

    Article Title: A Combination of Plant-Derived Extracts Modulates Nutrient-Responsive Metabolic Signalling in an In Vitro Gut–Liver–Adipose Model

    doi: 10.3390/nu18091393

    Figure Lengend Snippet: Mechanistic evaluation of combination treatment with the GLP-1R antagonist Exendin (9–39) on metabolic markers. Metabolic markers, including GLP-1R, AMPK, SIRT1, and resistin, were quantified in HepG2 cells, while SIRT1 and UCP-1 levels was evaluated in 3T3-L1 adipocytes. Specifically, in ( A ) GLP-1R levels; in ( B ) AMPK levels; in ( C ) SIRT1 levels (HepG2 cells); in ( D ) Resistin levels; in ( E ) UCP-1 levels; in ( F ) SIRT1 levels (3T3-L1 cells). The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) from 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. * p < 0.05 vs. control; φ p < 0.05 vs. PA.

    Article Snippet: Human HepG2 hepatocellular carcinoma cells (ATCC ® , Manassas, VA, USA) were used as an in vitro hepatic model to investigate glucose and lipid metabolic pathways.

    Techniques: Control

    Validation of GLP-1R-mediated signalling through rescue experiments with exogenous GLP-1 and Liraglutide (both at 100 nM). The contribution of the GLP-1R pathway was confirmed by co-treating cells with the botanical combination and either exogenous GLP-1 or a specific GLP-1R agonist (Liraglutide) in the presence of the antagonist Exendin(9–39). Metabolic markers, including GLP-1R, AMPK, SIRT1, and resistin, were quantified in HepG2 cells, while SIRT1 and UCP-1 levels was evaluated in 3T3-L1 adipocytes. Specifically, in ( A ) GLP-1R levels; in ( B ) AMPK levels; in ( C ) SIRT1 levels (HepG2); and in ( D ) Resistin levels; in ( E ) UCP-1 levels and in ( F ) SIRT1 levels (3T3-L1). The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) of 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. * p < 0.05 vs. control; φ p < 0.05 vs. PA.

    Journal: Nutrients

    Article Title: A Combination of Plant-Derived Extracts Modulates Nutrient-Responsive Metabolic Signalling in an In Vitro Gut–Liver–Adipose Model

    doi: 10.3390/nu18091393

    Figure Lengend Snippet: Validation of GLP-1R-mediated signalling through rescue experiments with exogenous GLP-1 and Liraglutide (both at 100 nM). The contribution of the GLP-1R pathway was confirmed by co-treating cells with the botanical combination and either exogenous GLP-1 or a specific GLP-1R agonist (Liraglutide) in the presence of the antagonist Exendin(9–39). Metabolic markers, including GLP-1R, AMPK, SIRT1, and resistin, were quantified in HepG2 cells, while SIRT1 and UCP-1 levels was evaluated in 3T3-L1 adipocytes. Specifically, in ( A ) GLP-1R levels; in ( B ) AMPK levels; in ( C ) SIRT1 levels (HepG2); and in ( D ) Resistin levels; in ( E ) UCP-1 levels and in ( F ) SIRT1 levels (3T3-L1). The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) of 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. * p < 0.05 vs. control; φ p < 0.05 vs. PA.

    Article Snippet: Human HepG2 hepatocellular carcinoma cells (ATCC ® , Manassas, VA, USA) were used as an in vitro hepatic model to investigate glucose and lipid metabolic pathways.

    Techniques: Biomarker Discovery, Control

    Protective effects against lipotoxicity markers in HepG2 cells. HepG2 cells were exposed to palmitic acid (PA) for 24 h to induce lipotoxicity followed by 24 h treatment with basolateral conditioned medium collected from the Transwell ® intestinal system. In ( A – E ) were reported the levels of signalling proteins and intracellular lipids quantified by ELISA: ( A ) Src, ( B ) GLP-1R, ( C ) triglycerides, ( D ) SREBP-1, and ( E ) AMPK. The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) of 5 independent experiments, each performed in triplicate, normalised to the control (0%) line. φ p < 0.05 vs. PA, * p < 0.05 vs. control, α p < 0.05 vs. single agents.

    Journal: Nutrients

    Article Title: A Combination of Plant-Derived Extracts Modulates Nutrient-Responsive Metabolic Signalling in an In Vitro Gut–Liver–Adipose Model

    doi: 10.3390/nu18091393

    Figure Lengend Snippet: Protective effects against lipotoxicity markers in HepG2 cells. HepG2 cells were exposed to palmitic acid (PA) for 24 h to induce lipotoxicity followed by 24 h treatment with basolateral conditioned medium collected from the Transwell ® intestinal system. In ( A – E ) were reported the levels of signalling proteins and intracellular lipids quantified by ELISA: ( A ) Src, ( B ) GLP-1R, ( C ) triglycerides, ( D ) SREBP-1, and ( E ) AMPK. The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) of 5 independent experiments, each performed in triplicate, normalised to the control (0%) line. φ p < 0.05 vs. PA, * p < 0.05 vs. control, α p < 0.05 vs. single agents.

    Article Snippet: Human HepG2 hepatocellular carcinoma cells (ATCC ® , Manassas, VA, USA) were used as an in vitro hepatic model to investigate glucose and lipid metabolic pathways.

    Techniques: Enzyme-linked Immunosorbent Assay, Control

    Comparative effects of individual extracts and their combination on metabolic signalling and oxidative stress markers. HepG2 cells were exposed to palmitic acid (PA) for 24 h to induce lipotoxicity followed by 24 h treatment with basolateral conditioned medium collected from the Transwell ® intestinal system. In ( A – E ) were reported the levels of signalling proteins quantified by ELISA assay: ( A ) SIRT1, ( B ) PGC1α, ( C ) Resistin, ( D ) FGF-21, and ( E ) NRF2. The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) from 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. φ p < 0.05 vs. PA, * p < 0.05 vs. control, α p < 0.05 vs. single agents.

    Journal: Nutrients

    Article Title: A Combination of Plant-Derived Extracts Modulates Nutrient-Responsive Metabolic Signalling in an In Vitro Gut–Liver–Adipose Model

    doi: 10.3390/nu18091393

    Figure Lengend Snippet: Comparative effects of individual extracts and their combination on metabolic signalling and oxidative stress markers. HepG2 cells were exposed to palmitic acid (PA) for 24 h to induce lipotoxicity followed by 24 h treatment with basolateral conditioned medium collected from the Transwell ® intestinal system. In ( A – E ) were reported the levels of signalling proteins quantified by ELISA assay: ( A ) SIRT1, ( B ) PGC1α, ( C ) Resistin, ( D ) FGF-21, and ( E ) NRF2. The Morus alba extract used in this study was obtained from leaves, the Paeonia lactiflora extract from roots, and the Gastrodia elata extract from rhizomes. Data are expressed as mean ± SD (%) from 5 independent experiments, each performed in triplicate and normalised to the control (0%) line. φ p < 0.05 vs. PA, * p < 0.05 vs. control, α p < 0.05 vs. single agents.

    Article Snippet: Human HepG2 hepatocellular carcinoma cells (ATCC ® , Manassas, VA, USA) were used as an in vitro hepatic model to investigate glucose and lipid metabolic pathways.

    Techniques: Enzyme-linked Immunosorbent Assay, Control