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目的初步探讨肝细胞生长因子(HGF)防护铅处理致人肾小球系膜细胞(HMC)损伤的作用机制。方法将HMC分为对照组(C组)、Pb 10μmol/L组和HGF+Pb 10μmol/L组,在6、12、24、48 h分别通过噻唑蓝(MTT)法检测细胞存活率和用流式细胞仪检测凋亡率;实时荧光定量-PCR检测各组细胞中Caspase-3的表达水平。结果 MTT检测结果显示,Pb 10μmol/L组HMC在6、12、24、48 h细胞生长存活率均显著低于HGF+Pb 10μmol/L组(P<0.01);流式凋亡检测结果显示,HMC在10μmol/L醋酸铅染毒6、12、24和48 h后,HGF+Pb 10μmol/L组在各个时间点细胞凋亡率显著低于Pb 10μmol/L组(P<0.01)。实时荧光定量-PCR检测结果显示,在HMC铅染毒48 h后,HGF+Pb 10μmol/L组Caspase-3的表达量显著低于Pb 10μmol/L组(P<0.01)。结论铅促进HMC细胞的凋亡,而HGF通过降低Caspase-3的表达抑制HMC的凋亡,从而发挥对铅致HMC细胞损伤的保护作用。
Objective To investigate the mechanism of lead injury induced by hepatocyte growth factor (HGF) in human mesangial cells (HMC). Methods HMCs were divided into control group (group C), Pb 10 μmol / L group and HGF + Pb 10 μmol / L group. Cell viability and flow cytometry were detected by MTT assay at 6, 12, 24, Apoptosis rate was detected by flow cytometry. The expression of Caspase-3 in each group was detected by real-time fluorescence quantitative-PCR. Results The results of MTT assay showed that the survival rate of HMCs in Pb 10μmol / L group was significantly lower than that in HGF + Pb 10μmol / L group (P <0.01) at 6, 12, 24 and 48 hours. The results of flow cytometry showed that, At 6, 12, 24 and 48 h after exposure to 10 μmol / L lead acetate, the apoptotic rate of HGF + Pb 10 μmol / L group was significantly lower than that of Pb 10 μmol / L group (P <0.01). The results of real-time fluorescence quantitative PCR showed that the expression of Caspase-3 in HGF + Pb 10 μmol / L group was significantly lower than that in Pb 10 μmol / L group (P <0.01) 48 h after HMC exposure. Conclusion Lead promotes the apoptosis of HMC cells, while HGF inhibits the apoptosis of HMC by decreasing the expression of Caspase-3, so that HGF can protect the HMC from lead-induced injury.