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虫草素对补体复合物介导的足细胞损伤的保护作用 被引量:10

Cordycepin Protects Podocytes from Injury Mediated by Complements Complex C5b-9
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摘要 目的探讨冬虫夏草的生物活性单体成分——虫草素(3′-脱氧腺苷)对补体介导的足细胞损伤的保护作用及其可能机制。方法补体复合物C5-9介导的足细胞损伤作为膜性肾病的体外模型。采用永生化的小鼠足细胞株MPC5建立细胞损伤模型,虫草素作为干预药物。用电镜观察细胞超微形态结构的变化,用免疫荧光染色观察细胞骨架F-actin结构和足细胞特异蛋白nephrin的表达,用Western blot检测信号通路丝裂原活化蛋白激酶(MAPK)磷酸化水平。结果 C5b-9刺激细胞3h后,细胞二级足突消失,细胞骨架结构明显损伤,F-actin应力纤维混乱,nephrin分布由胞膜移至胞浆,并引起p38、JNK、ERK磷酸化。虫草素能够保护足细胞的足突和细胞骨架结构,抑制nephrin的重分布,并显著抑制补体介导的p38/JNK信号通路活化。结论虫草素能保护足细胞对抗补体介导的损伤,其机制至少部分是通过抑制p38/JNK信号通路活化而实现的。 Objective To explore the protective effect of Cordycepin(3'-deoxyadenosine),a bioactive compound of Cordyceps Sinensis,on injury of podocytes.Methods C5b-9-induced podocyte injury was used as a model of membranous nephropathy in vitro.This model was established using mouse podocyte cell line——MPC5.Cordycepin was given as an intervention.Ultra-micro morphological changes were observed by electron microscope.F-actin cytoskeleton and expression of nephrin were observed by fluorescence microscope.The phosphorylation of mitogen-activated protein kinase(MAPK)was measured by Western blot.Results Stimulated by C5b-9for 3h,MPC5 showed secondary foot processes,with cytoskeleton structure damaged,nephrin relocated from the cell surface to the cytoplasm,and cell signal pathway-p38,JNK and ERK activated.Cordycepin protected foot processes and cytoskeleton structures of podocytes,suppressed the redistribution of nephrin,and inhibited p38/JNK action.Conclusion Cordycepin can protect podocyte from C5b-9-induced injury partly through inhibiting the activation of p38/JNK signaling pathway.
出处 《四川大学学报(医学版)》 CAS CSCD 北大核心 2015年第2期173-178,227,共7页 Journal of Sichuan University(Medical Sciences)
基金 四川省卫生厅科研基金(No.120331)资助
关键词 虫草素 足细胞 补体复合物 膜性肾病 MAPK Cordycepin Podocyte Complement complex Membranous nephropathy Mitogen-activated protein kinase
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