珍珠梅黄酮纳米粒抑制人肝癌HepG-2细胞STAT3诱导细胞凋亡

Apoptosis of human hepatocellular carcinoma HepG-2 cells upon inhibition of STAT3 by 5,2',4'-trihydroxy-6,7,5'-trimethoxy flavone nanoparticle

本文研究了珍珠梅黄酮纳米粒(5,2',4'-trihydroxy-6,7,5'-trimethoxyflavone nanoparticle,TTF1-NP)通过STAT3诱导人肝癌Hep G-2细胞凋亡的分子机制。MTT法、免疫细胞化学染色和流式细胞术结合Annexin VFITC/PI检测发现,TTF1-NP可明显抑制人肝癌Hep G-2细胞增殖,诱导细胞凋亡,且抑制作用呈浓度、时间依赖效应。免疫印迹结果显示,TTF1-NP下调survivin、p-STAT3和STAT3表达,上调cleaved caspase 3表达。采用si RNA沉默STAT3、脂质体转染STAT3载体表达质粒过表达STAT3技术,证明TTF1-NP可调控STAT3蛋白的表达,诱导细胞凋亡。结果表明:TTF1-NP通过抑制STAT3的表达,诱导人肝癌Hep G-2细胞凋亡。

This study was designed to investigate the mechanism of 5,2＇,4＇-trihydroxy-6,7,5＇-trimethoxy flavone nanoparticle（TTF1-NP） in the induction of apoptosis of human hepatocellular carcinoma HepG-2 cells. MTT assay, immunocytochemical staining and flow cytometry with Annexin V-FITC/PI were used to demonstrate inhibition of proliferation of HepG-2 cells and cell apoptosis. The inhibition was studied in a dose- and time-dependent manner. Western blot results showed that TTF1-NP down-regulated the signals of survivin, p-STAT3 and STAT3, but up-regulated the expression level of cleaved caspase-3. Taken together, our results showed that TTF1-NP induced HepG-2 cell apoptosis through inhibition of the STAT3 expression.