【摘要】 目的 研究雷公藤内酯醇（triptolide, TTL）对肝癌细胞糖代谢的调节作用及其促凋亡机制。方法 使用不同浓度（40、80、160 nmol/L）的TTL处理人肝癌HepG2细胞48 h。通过细胞计数试剂盒-8(CCK-8)和EdU染色检测细胞增殖能力；采用流式细胞术分析细胞凋亡水平；运用酶联免疫吸附实验（ELISA）测定葡萄糖摄取量、ATP生成量、乳酸生成量以及己糖激酶和丙酮酸激酶的活性；利用蛋白质免疫印迹法检测磷酸化Akt(p-Akt)和磷酸化mTOR(p-mTOR)的蛋白表达水平。结果 经雷公藤内酯醇处理后，HepG2细胞的增殖能力减弱，细胞凋亡水平升高。在糖代谢方面，细胞的葡萄糖摄取量、ATP生成量、乳酸生成量以及己糖激酶和丙酮酸激酶的活性均呈现下降趋势。同时，p-Akt和p-mTOR的蛋白表达水平降低。结论 雷公藤内酯醇可能通过抑制Akt/mTOR信号通路，降低肝癌细胞的糖代谢水平，从而促进其凋亡。更多还原

【Abstract】 Objective To investigate the regulatory effect of triptolide(TTL) on glucose metabolism in hepatocellular carcinoma HepG2 cells and its mechanism in promoting apoptosis. Methods HepG2 cells were treated with different concentrations(40, 80, and 160 nmol/L) of TTL for 48 hours. Cell proliferation ability was detected by Cell Counting Kit-8(CCK-8) and EdU staining; apoptosis levels were analyzed by flow cytometry; glucose uptake, ATP production, lactate production, and the activities of hexokinase and pyruvate kinase were measured using enzyme-linked immunosorbent assay(ELISA); the protein expression levels of phosphorylated Akt(p-Akt) and phosphorylated mTOR(p-mTOR) were determined by Western blot analysis. Results After TTL treatment, the proliferation of HepG2 cells decreased, while apoptosis levels increased. In terms of glucose metabolism, cellular glucose uptake, ATP production, lactate production, and the activities of hexokinase and pyruvate kinase all showed a declining trend. Meanwhile, the protein expression levels of p-Akt and p-mTOR were reduced. Conclusion Triptolide may promote apoptosis in hepatocellular carcinoma cells by inhibiting the Akt/mTOR signaling pathway and reducing glucose metabolism levels.更多还原