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: Oncology Reports

Article Title: Regorafenib and Nifuroxazide exert enhanced suppression of hepatocellular carcinoma by inhibiting STAT3 and immune remodeling

doi: 10.3892/or.2026.9074

Figure Lengend Snippet: Transcriptome analysis reveals the mechanisms underlying the enhanced efficacy of Regorafenib and Nifuroxazide in HCC. (A) Gene expression heatmap of key genes (including Vegfa, Bax and STAT3) in Regorafenib-treated compared with control HCC cells. (B) GSEA-based enrichment of Hallmark pathways in Regorafenib-treated HCC cells. (C) GSEA enrichment plot for the Hallmark_IL6_Jak_STAT3_Signaling pathway. (D) Representative results of the CCK-8 assay (for cell viability) of HepG2 cells under different treatments. (E) Statistical analysis of cell viability in . (F) Representative colony formation assay images of HepG2 cells under different treatments. (G) Statistical analysis of the number of colonies in . (H) Representative wound-healing assay images (0, 24 and 48 h) of HepG2 cells under different treatments. (I) Statistical analysis of wound closure rate in . Data are presented as mean ± standard deviation (n=3). *P<0.05 vs. the Control group; # P<0.05 vs. the Regorafenib group; $ P<0.05 vs. the Nifuroxazide group. HCC, hepatocellular carcinoma; GSEA, Gene Set Enrichment Analysis.

Article Snippet: Human HepG2 cells were authenticated by short tandem repeat (STR) profiling, which matched the reference STR data of ATCC HB-8065.

Techniques: Gene Expression, Control, CCK-8 Assay, Colony Assay, Wound Healing Assay, Standard Deviation

Journal: Oncology Reports

Article Title: Regorafenib and Nifuroxazide exert enhanced suppression of hepatocellular carcinoma by inhibiting STAT3 and immune remodeling

doi: 10.3892/or.2026.9074

Figure Lengend Snippet: Effects of different treatments on apoptosis and the expression of related proteins. (A) Effects of Nifuroxazide combined with Regorafenib on HepG2 cell apoptosis detected by flow cytometry. (B) Statistical analysis of . (C) Expression of related proteins in cells detected by western blotting. (D) Statistical analysis of . Data are presented as mean ± standard deviation (n=3). *P<0.05 vs. the Control group; # P<0.05 vs. the Regorafenib group; $ P<0.05 vs. the Nifuroxazide group. STAT3, signal transducer and activator of transcription 3; PD-L1, programmed death ligand 1; VEGF, vascular endothelial growth factor; p-, phosphorylated.

Article Snippet: Human HepG2 cells were authenticated by short tandem repeat (STR) profiling, which matched the reference STR data of ATCC HB-8065.

Techniques: Expressing, Flow Cytometry, Western Blot, Standard Deviation, Control

Journal: Biomedical Reports

Article Title: Targeting ULK1 and USP20 to modulate autophagy and chemosensitivity in cancer cell lines

doi: 10.3892/br.2026.2124

Figure Lengend Snippet: Changes in the basal autophagy flux in different cancer cell lines in response to doxorubicin. HepG2, MCF-7, MDA-MB-231, U87 and normal fibroblast cells were treated with different concentrations of doxorubicin chemotherapy. The level of expression of ULK1, USP20, and P62 was determined via reverse transcription-quantitative PCR. (A-C) Relative expression of ULK1, USP20 and P62 in HepG2 cells. (D-F) Relative expression of ULK1, USP20 and P62 in MCF-7 breast cancer cells. (G-I) Relative expression of ULK1, USP20 and P62 in MDA-MB-231 breast cancer cells. (J-L) Relative expression of ULK1, USP20 and P62 in U87 cells. (M-O) Relative expression of ULK1, USP20 and P62 in normal fibroblast cells. Three repeats were considered for each treatment group. Data are presented as the mean ± SEM. Statistical significance was indicated as * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001 (one-way ANOVA followed by Bonferroni's multiple comparisons post hoc test). ULK1, Unc-51-like kinase 1.

Article Snippet: The following cell lines were involved in the present study and provided from The American Type Culture Collection, human pancreatic cancer cell line PANC-1 (CRL-1469 TM ), Human lung carcinoma-A549 (CRM-CCL-185 TM ), human glioblastoma of unknown origin U-87 MG (HTB-14 TM ), human liver cancer HepG2 (HB-8065 TM ), human breast carcinoma MCF7 (HTB-22 TM ), human breast adenocarcinoma MDA-MB-231 (CRM-HTB-26 TM ), and human normal primary non-immortalized dermal fibroblasts-HDFa (PCS-201-012, https://www.atcc.org/products/pcs-201-012 ).

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction

Journal: Journal of Advanced Research

Article Title: The GOLM1-ACLY pathway regulates macrophage-secreted EFEMP1 via H3K27ac modifications to drive tumor progression

doi: 10.1016/j.jare.2025.07.003

Figure Lengend Snippet: EFEMP1 promotes the proliferation activity in tumor cells cocultured with Golm1 -knockout macrophages via EGFR-AKT/MAPK signaling (A) Immunoblot detection of EFEMP1 protein expression of in Thp1 nc and Thp1 −/− cells cocultured with HepG2. (B) ELISA assay of the EFEMP1 content in the supernatants harvested from Thp1 nc or Thp1 −/− cocultured with HepG2 respectively. n = 4 samples/group. (C) Immunoblot detection of EFEMP1 protein expression in different treated Thp1 cells. (D) ELISA assay of EFEMP1 content in the supernatants harvested from different treated Thp1 cocultured with HepG2. n = 4 samples/group. (E) Immunoblot detection of the EGFR expression in HepG2 cocultured with Thp1 nc or Thp1 −/− cells. (F) Immunoblot detection of the AKT and MAPK protein levels in HepG2 cocultured with Thp1 nc or Thp1 −/− cells. (G and H) Immunoblot analysis of the indicated protein levels in HepG2 cocultured with different treated Thp1 cells. (I) Schematic representation of the different treated-Thp1-Huh7 admixture tumor model on nude mice. (J) Tumor growth curves of subcutaneous models involving Huh7 cells cocultured with different treated-Thp1 cells. n = 5 nude mice per group. (K) Tumor weight of subcutaneous tumor in groups of nude mice. n = 5 nude mice. (L) Immunoblot detection of the AKT and MAPK protein levels in subcutaneous tumors. All blots are representative of 3 independent experiments. The data are presented as the means ± SEMs. Statistical significance was determined by two-tailed Student's t test (B) and one-way ANOVA followed by Tukey's multiple comparisons test (D, J, and K). ns, not statistically significant. *p < 0.05; **p < 0.01; ***p < 0.001.

Article Snippet: The human HCC cell lines Huh7 and HepG2; the human macrophage lines Thp1and HEK293T and the mouse liver cancer cell line Hepa1-6 were originally obtained from the ATCC.

Techniques: Activity Assay, Knock-Out, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test