【摘 要】
：
目的 观察祛风通络配伍对高糖诱导人肾小管上皮细胞(human renal tubular epithelial cell,HKC)活力及炎症反应的影响.方法 体外培养HKC并采用高糖DMEM培养基诱导其增殖,设立正常组、模型组、抑制剂组、祛风通络组,CCK-8法测定各组细胞的活力;酶联免疫吸附测定法检测白细胞介素1β(interleukin 1β,IL-1β)、白细胞介素6(interleukin 6,IL-6)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)的含量;逆转录—
【机 构】
：
100700 北京中医药大学第一临床医学院;北京中医药大学东直门医院肾病内分泌科;北京中医药大学中医学院;北京中医药大学东直门医院肾病内分泌科
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目的 观察祛风通络配伍对高糖诱导人肾小管上皮细胞(human renal tubular epithelial cell,HKC)活力及炎症反应的影响.方法 体外培养HKC并采用高糖DMEM培养基诱导其增殖,设立正常组、模型组、抑制剂组、祛风通络组,CCK-8法测定各组细胞的活力;酶联免疫吸附测定法检测白细胞介素1β(interleukin 1β,IL-1β)、白细胞介素6(interleukin 6,IL-6)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)的含量;逆转录—聚合酶链式反应(RT-PCR)法测定IL-1β、IL-6、TNF-α、细胞间黏附分子-1(intercellular adhesion molecule 1,ICAM-1)、单核细胞趋化蛋白-1(monocyte chemoattractant protein 1,MCP-1)、p38丝裂原活化蛋白激酶(p38 mitogen activated protein kinase,p38 MAPK)的mRNA的表达;蛋白免疫印迹法检测p38 MAPK、ICAM-1、MCP-1的蛋白表达水平.结果 与正常组比较,模型组细胞活力显著下降(P<0.05),IL-1β、IL-6、TNF-α的含量增加(P<0.05),IL-1β、IL-6、TNF-α、ICAM-1、MCP-1、p38 MAPK的mRNA表达增加(P<0.05),p38 MAPK、ICAM-1、MCP-1蛋白的表达增加(P<0.05);与模型组比较,抑制剂组和祛风通络组细胞活力显著增高(P<0.05),IL-1β、IL-6、TNF-α的含量降低(P<0.05),IL-1β、IL-6、TNF-α、ICAM-1、MCP-1、p38 MAPK mRNA的表达降低(P<0.05),MCP-1、p38 MAPK、ICAM-1蛋白的表达减少(P<0.05).结论 祛风通络配伍可以明显提高高糖诱导HKC的细胞活力,并可能通过作用于p38 MAPK信号通路减少IL-1β、IL-6、TNF-α、MCP-1、ICAM-1的表达,进而减轻炎症反应.
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