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探讨珍珠梅黄酮纳米粒(5,2’,4’-trihydroxy-6,7,5’-trimethoxy flavone nanoparticle,TTF1-NP)抑制脂多糖(lipopoiysaccharide,LPS)诱发人肝癌HepG2细胞的炎性作用及调控机制。采用LPS诱发人肝癌HepG2细胞的炎症模型;MTT比色法检测TTF1-NP对人肝癌HepG2细胞增殖作用;Western blot法检测TTF1-NP对LPS诱发的HepG2细胞炎性反应的TLR4和IL-6及AKT/m TOR信号通路关键蛋白的表达作用。结果显示,TTF1-NP能够抑制LPS引起的人肝癌HepG2细胞增殖,抑制TLR4蛋白表达及AKT和m TOR蛋白的磷酸化,抑制炎症因子IL-6和IL-8表达;TTF1-NP抑制胰岛素引起的AKT/m TOR信号通路的活化和TLR4蛋白的表达,从而降低IL-6和IL-8蛋白水平。研究表明,TTF1-NP抑制LPS诱导的人肝癌HepG2细胞的炎性反应,其作用机制可能与AKT/m TOR信号通路有关。
To investigate the inflammatory effect of 5,2 ’, 4’-trihydroxy-6,7,5’-trimethoxythiopentone nanoparticle (TTF1-NP) on HepG2 cells induced by lipopoiysaccharide (LPS) Regulatory mechanism. The LPS-induced human hepatocellular carcinoma HepG2 cell inflammatory model; MTT colorimetric assay TTF1-NP on human hepatocellular carcinoma HepG2 cell proliferation; Western blot method to detect TTF1-NP on LPS-induced HepG2 inflammatory response TLR4 and IL-6 and AKT / m TOR signaling pathway key protein expression. The results showed that TTF1-NP could inhibit the proliferation of HepG2 cells induced by LPS, inhibit the expression of TLR4 protein, AKT and mTOR protein phosphorylation, and suppress the expression of inflammatory cytokines IL-6 and IL-8. TTF1-NP inhibited insulin-induced AKT / m TOR signaling pathway activation and TLR4 protein expression, thereby reducing IL-6 and IL-8 protein levels. Studies have shown that, TTF1-NP inhibit LPS-induced human hepatocellular carcinoma HepG2 inflammatory response may be related to AKT / m TOR signaling pathway.