哈尔滨商业大学学报（自然科学版）2026，Vol.42Issue(4)：387-391,5.
海南地不容氧化克班宁调控PDK1/AKT通路诱导HepG-2细胞自噬机制
Study on mechanism of oxocrebanine from Stephania hainanensis inducing autophagy in human hepatocellular carcinoma HepG-2 cells via PDK1/AKT signaling pathway
摘要
Abstract
Based on previous findings that oxocrebanine from Stephania hainanensis H.S.Lo et Y.Tsoong(a Li ethnic medicine)induces autophagy in human hepatocellular carcinoma HepG-2 cells,this study further investigated the molecular mechanism,with a focus on verifying the regulatory role of phosphoinositide-dependent kinase-1(PDK1)-protein kinase B(Akt)signaling pathway in oxocrebanine-induced autophagy.The PDK1 gene was overexpressed in HepG-2 cells using liposome transfection to reversely validate the autophagic mechanism induced by oxocrebanine.Following treatment with oxocrebanine,the protein expression levels of the autophagy marker LC3-Ⅱ/LC3-Ⅰ ratio,total AKT,and phosphorylated AKT at Ser473(p-AKT)were detected by Western blotting.The results showed that oxocrebanine significantly increased the LC3-Ⅱ/LC3-Ⅰ ratio as well as the protein expression levels of AKT and p-AKT in PDK1-overexpressing cells,with extremely significant differences compared to the control group(P<0.01).In conclusion,oxocrebanine may activate the PDK1 signaling axis,promote AKT phosphorylation,and subsequently accelerate the conversion of LC3-Ⅰ to LC3-Ⅱ,ultimately inducing autophagy in HepG-2 cells.These findings provide new experimental evidence for the anti-hepatocellular carcinoma activity of active components derived from the Li ethnic medicine Stephania hainanensis.关键词
海南地不容氧化克班宁/HepG-2细胞/细胞自噬/LC3-Ⅱ/LC3-Ⅰ/PDK1/AKT通路Key words
oxocrebanine from Stephania hainanensis H.S.Lo et Y.Tsoong/HepG-2 cells/autophagy/LC3-Ⅱ/LC3-Ⅰ/PDK1/AKT signaling pathway分类
医药卫生引用本文复制引用
王正文,许声江,王先正,廖辉,张彩云,张小坡,赵艳,于蕾..海南地不容氧化克班宁调控PDK1/AKT通路诱导HepG-2细胞自噬机制[J].哈尔滨商业大学学报（自然科学版）,2026,42(4):387-391,5.基金项目
国家自然科学基金项目(82560834) （82560834）
海南省卫生健康科技创新联合项目(WSJK2024MS162) （WSJK2024MS162）
黑龙江自然科学基金项目(PL2025H212) （PL2025H212）
黑龙江省中医药科研课题(ZHY2024-098) （ZHY2024-098）
