cell culture human hepatocellular carcinoma cell lines hepg2  (ATCC)

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

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

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

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

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

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

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

Journal: bioRxiv

Article Title: An LSEC-focused computational drug repurposing platform for liver fibrosis: Identification of vorinostat and other LSEC-protective candidates

doi: 10.64898/2026.05.23.727430

Figure Lengend Snippet: (A) Summary of hepatocyte-derived factors in intercellular crosstalk during NAFLD pathogenesis. (B) Asah1 floxed ( Asah1 fl/fl /WT) mice and Asah1 fl/fl / Alb Cre mice (hepatocyte-specific deletion of Asah1 ) were fed with PD for 20 weeks. Hepatic and plasma HMGB1 levels were measured by ELISA. Hepatic HMGB1 level was normalized to total protein. (C) HepG2-hepatocytes were transfected with siNC or si ASAH1 for 48 hours, followed by treatment with vehicle or a lipid mixture consisting of free FAs (300 μM; OA: PA = 2:1) and 7K (40 μM) for 24 hours. Cell lysate and supernatant HMGB1 levels were quantified by ELISA. (D) Transwell co-culture schematic. HepG2 hepatocytes were cultured in the upper chamber, transfected with siNC or siASAH1 for 48 hours. Primary LSECs were cultured separately in the lower chamber. After transfection, co-culture was initiated with FA + 7K treatment in the upper chamber and vehicle or glycyrrhizin (60 μM, HMGB1 inhibitor) in the lower chamber for 24 hours. (E) qPCR quantification (normalized to HPRT1 ) and (F) heatmap of LSEC marker expression. Mean ± SEM; n = 4. * p < 0.05, ** p < 0.01. Abbreviations: HMGB1, high mobility group box 1; HSCs, hepatic stellate cells; RAGE, receptor for advanced glycation end products; pMEK1/2, phosphorylated mitogen-activated protein kinase kinase 1/2; pERK1/2, phosphorylated extracellular signal-regulated kinase 1/2; CCl₄, carbon tetrachloride; TAA, thioacetamide; BDL, bile duct ligation; ASH, alcoholic steatohepatitis; MCD, methionine-choline-deficient; NASH, nonalcoholic steatohepatitis; Hmgb1ΔHepΔMye, hepatocyte and myeloid cell-specific HMGB1 knockout; SHH, Sonic hedgehog; IHH, Indian hedgehog; TAZ, transcriptional co-activator with PDZ-binding motif (WWTR1); TEAD, TEA domain transcription factor; OPN, osteopontin; CEBPA, CCAAT/enhancer-binding protein alpha; EVs, extracellular vesicles; PPAR-γ, peroxisome proliferator-activated receptor gamma; α-SMA, alpha-smooth muscle actin; TIMP-2, tissue inhibitor of metalloproteinase 2; VEGF-A, vascular endothelial growth factor A; PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; VEGFR-2, vascular endothelial growth factor receptor 2; mAb, monoclonal antibody; VWF, von Willebrand factor; eNOS, endothelial nitric oxide synthase; ITGβ1, integrin beta 1; ITGα9β1, integrin alpha 9 beta 1; VCAM-1, vascular cell adhesion molecule 1; MoMF, monocyte-derived macrophage; CCL2, C-C motif chemokine ligand 2; RBPJ, recombination signal binding protein for immunoglobulin kappa J region; MCP-1, monocyte chemoattractant protein-1; CCR2, C-C motif chemokine receptor 2; IRE1α, inositol-requiring enzyme 1 alpha; S1P, sphingosine-1-phosphate; S1PR1, sphingosine-1-phosphate receptor 1; FOXO1, forkhead box O1; CXCL10, C-X-C motif chemokine ligand 10; MLK3, mixed lineage kinase 3; TRAIL, TNF-related apoptosis-inducing ligand; DR5, death receptor 5; RIP1, receptor-interacting protein 1; mtDNA, mitochondrial DNA; TLR9, Toll-like receptor 9; FA, fatty acid; 7K, 7-ketocholesterol; siNC, negative control siRNA; siASAH1, ASAH1 siRNA; Gly, Glycyrrhizin; HPRT1, hypoxanthine phosphoribosyltransferase; NLRP3, NLR family pyrin domain containing 3; CASP1, caspase-1; ICAM1, intercellular adhesion molecule 1; GSDMD, gasdermin D; LYVE1, lymphatic vessel endothelial hyaluronan receptor 1; KDR, kinase insert domain receptor; PLVAP, plasmalemma vesicle-associated protein; COL4A1, collagen type IV alpha 1 chain; COL4A2, collagen type IV alpha 2 chain; TGF-β, transforming growth factor beta; MMP2, matrix metallopeptidase 2; MMP9, matrix metallopeptidase 9; NOS3, nitric oxide synthase 3; ET-1, endothelin-1.

Article Snippet: Human hepatocellular carcinoma cell line HepG2 was purchased from ATCC and maintained in Eagle’s minimum essential medium (EMEM) with 10% FBS.

Techniques: Derivative Assay, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Transfection, Co-Culture Assay, Cell Culture, Marker, Expressing, Ligation, Knock-Out, Binding Assay, Negative Control

Journal: Frontiers in Nutrition

Article Title: Hongjam, an edible silkworm-derived food, attenuates steatohepatitis and fibrosis via multi-axis modulation of metabolic stress, inflammation, and fibrogenic signaling

doi: 10.3389/fnut.2026.1839551

Figure Lengend Snippet: Silk fibroin peptides suppress inflammatory signaling and modulate TGF-β/Smad-associated responses in vitro . (A) In LPS-stimulated RAW264.7 cells, fibroin peptides reduce phosphorylation of IκBα and p65, and suppress COX-2 and iNOS expression. (B) In TGF-β–stimulated HepG2 cells, fibroin peptides attenuate p-SMAD3 and α-SMA protein expression. (C) qRT–PCR analysis shows reduced expression of TGF-β1, α-SMA, SNAIL, MMP2, and TNF-α transcripts following fibroin peptide treatment. Data are presented as mean ± s.d. from three independent experiments (each in triplicate). Statistical significance was determined by one-way ANOVA followed by Tukey’s multiple comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control (untreated); # p < 0.05, ## p < 0.01, ### p < 0.001 vs. LPS- or TGF-β–treated group.

Article Snippet: Murine RAW 264.7 macrophages (ATCC TIB-71; RRID: CVCL_0493) and human HepG2 hepatocellular carcinoma cells (ATCC HB-8065; RRID: CVCL_0027) were purchased from the Korean Cell Line Bank (KCLB) and maintained in accordance with KCLB’s guidelines.

Techniques: In Vitro, Phospho-proteomics, Expressing, Quantitative RT-PCR, Control

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