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目的观察重组腺病毒介导肝细胞生长因子基因(Ad-HGF)对铅致动脉内皮细胞损伤的保护作用,为Ad-HGF保护血脑屏障提供理论依据。方法实验设正常组、转染组、铅染组、转染加铅染毒组。转染加铅染毒组用Ad-HGF转染动脉内皮细胞48 h后,加入20μmol/L的醋酸铅,24 h、48 h后分别用G iem sa染色法观察细胞形态学变化;细胞免疫化学法检测P53的表达;流式细胞仪检测细胞凋亡率。结果染色显示出铅单独染毒组细胞成凋亡形态学改变。转染加铅染毒组动脉内皮细胞的免疫化学结果显示P53阳性表达较对照组下降。MTT结果表明铅处理不同时间点(6 h、12 h、18 h、24 h、48 h)后,转染加铅染毒组细胞增殖率与铅单独染毒组比较没有显著升高(P>0.05),转染组的增殖率略高于对照组(P<0.05)。醋酸铅组细胞凋亡率较对照组明显升高,转染组较未转染组比较细胞凋亡率明显下降。结论 Ad-HGF具有抗细胞凋亡作用,为解释Ad-HGF对铅致血脑屏障的损伤保护效应提供有力的理论和实验依据。
Objective To observe the protective effect of recombinant adenovirus-mediated hepatocyte growth factor gene (Ad-HGF) on the injury of lead-induced arterial endothelial cells and provide a theoretical basis for the protection of blood-brain barrier by Ad-HGF. Methods The experiment set up normal group, transfection group, lead group, transfection plus lead group. Transfected plus lead-exposed group were transfected with Ad-HGF for 48 h, then added 20 μmol / L lead acetate for 24 h and 48 h, respectively. The morphological changes were observed by Giemsa staining. Cell immunochemistry P53 expression was detected by flow cytometry apoptosis rate. Results The staining showed that the cells exposed to lead alone changed into apoptotic morphology. Immunochemical results of transfection plus lead-exposed group showed that the positive expression of P53 was lower than that of the control group. MTT results showed that the proliferation rate of transfected with lead-exposed group did not significantly increase compared with that of lead-exposed group after exposure to different time points (6 h, 12 h, 18 h, 24 h, 48 h) 0.05). The proliferation rate in transfection group was slightly higher than that in control group (P <0.05). The apoptosis rate of lead acetate group was significantly higher than that of control group, the apoptosis rate of transfected group was significantly decreased compared with untransfected group. Conclusions Ad-HGF has anti-apoptotic effects, providing a powerful theoretical and experimental basis for explaining the protective effect of Ad-HGF on lead-induced blood-brain barrier injury.