Effect of metformin on cell proliferation and apoptosis in steatosis HepG2 cell model.

IF 0.9
Northern clinics of Istanbul Pub Date : 2025-08-11 eCollection Date: 2025-01-01 DOI:10.14744/nci.2024.49775
Ayse Melek Tanriverdi Bademci, Banu Aydin, Hulya Cabadak
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Abstract

Objective: Metformin, which is commonly recommended drug for managing type II diabetes, has been reported to have anti-cancer properties and may improve the prognosis of some malignancies. Epidemiology studies have shown improved survival in cancer patients using metformin. However, the mechanism behind this phenomenon remains incompletely understood. In our study, Our objective was to investigate how metformin influences the proliferation and apoptosis of hepatocellular carcinoma cells induced with steatosis via palmitic acid and oleic acid.

Methods: We established an in vitro cellular model of non-alcoholic fatty liver disease by inducing lipid accumulation in HepG2 cells through the use of oleic acid and palmitic acid. Oil Red O staining was conducted to observe the distribution of intracellular lipid droplets. Cell proliferation were detected using the BrdU cell proliferation detection kit. Protein expressions were detected by western blot method techniques.

Results: We found that metformin reduced cell proliferation in palmitic acid and oleic acid-induced HepG2 cells compared to the control group. Moreover, our western blot data show that metformin treatment changes apoptosis.

Conclusion: Our results show that metformin inhibits cell viability of steatosis HepG2 cells. These findings may be preliminary for new studies in steatosis HepG2 cells and may provide new therapeutic targets or treatment strategies against hepatocellular carcinoma.

二甲双胍对脂肪变性HepG2细胞增殖和凋亡的影响。
目的:二甲双胍是治疗II型糖尿病的常用推荐药物,有报道称其具有抗癌特性,并可能改善某些恶性肿瘤的预后。流行病学研究表明,使用二甲双胍可以提高癌症患者的生存率。然而,这种现象背后的机制仍然不完全清楚。在我们的研究中,我们的目的是研究二甲双胍如何影响棕榈酸和油酸诱导的肝细胞脂肪变性细胞的增殖和凋亡。方法:利用油酸和棕榈酸诱导HepG2细胞脂质积累,建立非酒精性脂肪肝体外细胞模型。油红O染色观察细胞内脂滴分布。采用BrdU细胞增殖检测试剂盒检测细胞增殖情况。western blot法检测蛋白表达。结果:我们发现与对照组相比,二甲双胍降低了棕榈酸和油酸诱导的HepG2细胞的细胞增殖。此外,我们的western blot数据显示,二甲双胍治疗改变了细胞凋亡。结论:二甲双胍抑制脂肪变性HepG2细胞活力。这些发现可能为脂肪变性HepG2细胞的新研究奠定了基础,并可能为肝癌的治疗提供新的靶点或治疗策略。
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