ChREBP在HepG2肝癌细胞糖脂代谢紊乱中的调控作用  

The regulatory role of ChREBP in the disorder of glucose and lipid metabolism in HepG2 liver cancer cells

作　　者：曾炼坤 邱友燕 蒋婵 熊静妮 陈丹丹 李素燕 刘雪芳 Zeng Liankun;Qiu Youyan;Jiang Chan(Department of Endocrinology,Fourth Affiliated Hospital of Guangzhou Medical University,Guangzhou 511300)

机构地区：[1]广州医科大学附属第四医院内分泌科,广东广州511300

出　　处：《中国现代医药杂志》2023年第10期20-23,共4页Modern Medicine Journal of China

基　　金：广州市科技计划项目资助(编号:202102080534)。

摘　　要：目的 探讨碳水化合物反应元件结合蛋白(ChREBP)在HepG2肝癌细胞糖脂代谢紊乱中的调控作用。方法 分别以18mmol/L和25mmol/L葡萄糖培养HepG2肝癌细胞,以11mmol/L葡萄糖培养HepG2肝癌细胞作为对照,测定三酰甘油(Triacylglycerol,TG)的含量、油红-O染色,以了解HepG2肝癌细胞脂肪变性的情况。采用免疫荧光法检测ChREBP入核。采用RT-PCR和Western blot技术分别测定不同浓度的肝型丙酮酸激酶(LPK)和脂肪酸合酶(FAS)的表达。结果 与对照组比较,经高糖处理后,HepG2肝癌细胞中的脂肪含量明显升高;高糖组在24h、48h HepG2肝癌细胞FAS蛋白的表达量分别为0.376±0.026、0.525±0.022,明显高于对照组的0.257±0.018、0.255±0.022,差异有统计学意义(P均<0.05);伴随着ChREBP的核转位,高糖组LPK基因mRNA及FAS蛋白的表达显著高于对照组。结论 葡萄糖的代谢物可通过ChREBP-LPK-FAS通路引起肝脏脂质沉积。Objective To investigate the regulatory role of ChREBP in the disorder of glucose and lipid metabolism in HepG2 liver cancer cells.Methods HepG2 liver cancer cells were cultured with 18mmol/L and 25mmol/L glucose,respectively.HepG2 liver cancer cells were cultured with 11mmol/L glucose as a control,and the content of triglycerides(TG)and oil red O staining were measured to understand their steatosis.Immunofluorescence assay was used to detect ChREBP entry into the nucleus.The expressions of hepatic pyruvate kinase(LPK)and fatty acid synthase(FAS)in different concentrations were measured by RT-PCR and Western blot.Results Compared with the control group,after high glucose treatment,the fat content in HepG2 liver cancer cells significantly increased.The expression levels of FAS protein in HepG2 liver cancer cells in the high glucose group at 24h and 48h were 0.376±0.026 and 0.525±0.022,which were significantly higher than those in the control group 0.257±0.018 and 0.255±0.022(all P<0.05).With the nuclear translocation of ChREBP,the expression of LPK gene mRNA and FAS protein in the high glucose group were significantly higher than those in the control group.Conclusion Metabolites of glucose can cause liver lipid deposition through the ChREBP-LPK-FAS pathway.

关 键 词：碳水化合物反应元件结合蛋白 HEPG2肝癌细胞 高糖 肝细胞脂肪变性 

分 类 号：R735.7[医药卫生—肿瘤]