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目的:探讨MSN对血管紧张素Ⅱ诱导的人胚肾成纤维细胞(HEK293)ColⅠ表达的影响。方法:将浓度为1×108/L的HEK293细胞悬液接种1mL在6孔板中1cm×1cm的打胶盖玻片上,用透射电镜观察细胞超微结构,同步化细胞后分为正常对照组,阳性对照组,MSN高、中、低剂量组和溶液对照组,各组加入相应药物干预24h,免疫组化法检测ColⅠ表达,将染色后的细胞爬片应用病理图集采集和分析系统软件半定量分析结果。结果:ColⅠ在正常人胚肾成纤维细胞包浆呈弱阳性含量,在阳性对照组AngⅡ刺激下呈强阳性含量;MSN高、中、低剂量组与阳性对照组相比,胞浆颜色均变淡,表达变弱,MSN低剂量组与溶液对照组无明显差异。ColⅠ光密度值阳性对照组高于正常对照组(P<0.05);MSN各剂量组均低于阳性对照组(P<0.05)。结论:MSN通过抑制ColⅠ的含量,从而抑制系膜基质增生,抑制慢性肾衰的纤维化发生和进展。
Objective: To investigate the effect of MSN on Col Ⅰ expression induced by angiotensin Ⅱ in human embryonic kidney fibroblast (HEK293). Methods: The HEK293 cell suspension with a concentration of 1 × 108 / L was inoculated with 1 mL of 1 cm × 1 cm plastic coverslips in a 6-well plate. The ultrastructure of the HEK293 cells was observed by transmission electron microscopy. The cells were synchronized and divided into normal control group , Positive control group, MSN high, medium and low dose groups and solution control group. Each group was treated with the corresponding drugs for 24 hours. Immunohistochemistry was used to detect the expression of ColⅠ. The stained cell slides were collected and analyzed with the pathology atlas Semi-quantitative analysis of the results. Results: ColⅠwas weakly positive in the plasma of normal human embryonic kidney fibroblasts and strongly positive in the positive control group (AngⅡ). Compared with the positive control group, the cytoplasm color of Col Ⅰ Light, weak expression, MSN low-dose group and solution control group no significant difference. Col Ⅰ optical density positive control group was higher than the normal control group (P <0.05); MSN dose groups were lower than the positive control group (P <0.05). Conclusion: MSN suppresses the proliferation of mesangial matrix and inhibits the occurrence and progression of fibrosis in chronic renal failure by inhibiting the content of ColⅠ.