摘要
目的:探讨黄芪多糖对糖尿病肾病肾小管上皮细胞凋亡、转分化及ROS含量的影响。方法:HK-2细胞分为低糖组、高糖组和黄芪多糖+高糖组,处理细胞48 h后,CCK-8实验检测细胞增殖;流式细胞仪检测细胞凋亡及ROS含量;Western blot检测E-cadherin、α-SMA、STAT1、STAT3、p-STAT1、p-STAT3蛋白表达。结果:高糖组细胞存活率显著低于低糖组(P<0.01),细胞凋亡率、ROS含量及E-cadherin、α-SMA、p-STAT1、p-STAT3蛋白表达均显著高于低糖组(P<0.01),高糖+黄芪多糖组细胞存活率显著高于高糖组,细胞凋亡率、ROS含量及E-cadherin、α-SMA、p-STAT1、p-STAT3蛋白表达均显著低于高糖组(P<0.01)。结论:黄芪多糖可促进高糖诱导的肾小管上皮细胞增殖,抑制细胞凋亡及转分化,其机制与下调JAK/STAT信号通路有关。
Objective:To investigate the effect of Astragalus polysaccharides on apoptosis,transdifferentiation and ROS content in renal tubular epithelial cells of diabetic nephropathy.Methods:HK-2 cells were divided into low glucose group,high glucose group and astragalus polysaccharide+high glucose group,cell proliferation was detected by CCK-8 assay after 48 h;cell apoptosis and ROS content was detected by flow cytometry;the expression of E-cadherin,α-SMA,STAT1,STAT3,p-STAT1,p-STAT3 protein were detected by Western blot.Results:The survival rate of cells in high glucose group was significantly lower than low sugar group(P<0.01),cell apoptosis rate,ROS content and E-cadherin,α-SMA,p-STAT1 and p-STAT3 protein expression was significantly higher than low sugar group(P<0.01),the cell survival rate in high glucose+astragalus polysaccharide group was significantly higher than high glucose group,cell apoptosis rate,ROS content and E-cadherin,α-SMA,p-STAT1 and p-STAT3 protein expression was significantly lower than high glucose group(P<0.01).Conclusion:Astragalus polysaccharides can promote the proliferation of renal tubular epithelial cells induced by high glucose,inhibit apoptosis and transdifferentiation,and the mechanism is related to down regulation of JAK/STAT signaling pathway.
作者
郭晓玲
康丽霞
任美芳
檀金川
GUO Xiao-Ling;KANG Li-Xia;REN Mei-Fang;TAN Jin-Chuan(Nephropathy of Department,Hebei Hospital of Traditional Chinese Medicine,Shijiazhuang 050011,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2018年第3期388-392,共5页
Chinese Journal of Immunology
关键词
黄芪多糖
糖尿病肾病
肾小管上皮细胞
Astragalus polysaccharides
Diabetic nephropathy
Renal tubular epithelial cells