山东医药2023，Vol.63Issue(33)：7-10,4.DOI:10.3969/j.issn.1002-266X.2023.33.002
依匹哌唑对结肠癌细胞系HCT116和SW620细胞内胆固醇合成的影响及其机制
Effect and mechanism of brexpiprazole on cholesterol synthesis of human colorectal cancer cell lines HCT116 and SW620
摘要
Abstract
Objective To observe the effect of brexpiprazole on cholesterol synthesis in colorectal cancer cell lines HCT116 and SW620,and to explore its mechanism.Methods HCT116 and SW620 cells in the logarithmic growth phase were divided into the brexpiprazole group and control group,respectively.Cells in the brexpiprazole group were add-ed with medium containing 20 μmol/L brexpiprazole,while cells in the control group were added with equal amount of me-dium.After the cells were cultured for 24 h,the total cholesterol(TC)in the cells was detected by microplate assay.Hu-man 3-hydroxy-3-methylglutaryl-CoA reductase(HMGCR)mRNA and human 3-hydroxy-3-methylglutaryl-CoA synthase 1(HMGCS1)mRNA were detected by real-time fluorescence quantitative PCR.HMGCR,HMGCS1,p-PI3K,p-AKT,and SREBP2 proteins were detected by Western blotting.Results The TC levels of HCT116 and SW620 cells were lower in the brexpiprazole group than in the control group(both P<0.05).The relative expression levels of HMGCR mRNA and HMGCS1 mRNA in HCT116 and SW620 cells in the brexpiprazole group were lower than those in the control group(all P<0.05).The relative protein expression levels of HMGCR,HMGCS1,p-PI3K,p-AKT and SREBP2 in HCT116 and SW620 cells of the brexpiprazole group were lower than those of the control group(all P<0.05).Conclusion Brexpipra-zole inhibits intracellular cholesterol synthesis in HCT116 and SW620 cells possibly by inhibiting the protein expression of PI3K/Akt-SREBP2 signaling pathway.关键词
依匹哌唑/结肠癌细胞/总胆固酮/PI3K/Akt-SREBP2信号通路Key words
brexpiprazole/colorectal cancer cells/total cholesterol/PI3K/Akt-SREBP2 singling pathway分类
医药卫生引用本文复制引用
李婷,龙小艺,刘肖洁,陈卫..依匹哌唑对结肠癌细胞系HCT116和SW620细胞内胆固醇合成的影响及其机制[J].山东医药,2023,63(33):7-10,4.基金项目
南充市2022年市校科技战略合作专项(22SXQT0332). （22SXQT0332）
