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白藜芦醇苷对缺氧复氧HK2细胞损伤保护作用的研究 被引量:8

Protective effect of polydatin on hypoxia/re-oxygenation induced HK2 cell injury
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摘要 目的探讨白藜芦醇苷(polydatin,PD)对缺氧复氧(hypoxia/re-oxygenation,H/R)肾小管上皮细胞损伤的保护作用。方法在缺氧仓中充入95%N2、5%CO2混合气体模拟缺氧环境,将人近曲肾小管上皮细胞(human kidney proxi-mal tubular epithelial cell,HK2)根据不同处理分为4组:正常对照组、H/R组、PDTC组和PD处理组,除对照组外每组均予以先缺氧24h后复氧6h处理;MTT法检测细胞成活数,免疫组化法检测NF-κBp65蛋白表达情况,RT-PCR检测ICAM-1 mRNA转录,ELISA法检测ICAM-1蛋白表达情况。结果PD处理组各对应时间点HK2细胞数量明显增多于H/R组,统计学差异显著(P<0.05)。PD处理组NF-κBp65蛋白阳性表达,ICAM-1 mRNA转录及ICAM-1蛋白表达均明显低于对照组,有统计学差异(P<0.05)。PD处理组与PDTC组各对应时间点的各项检测指标比较均无显著统计学差异(P>0.05)。结论PD对H/R诱导的HK2细胞损伤具有一定的保护作用。 Objective To study the protective effect of polydatin (PD) on hypoxia/re-oxygenation induced HK2 cell injury in vitro. Methods Human kidney proximal tubular epithelial cell line HK2 cell was used as target cell. The cells were divided into 4 groups : control group, model group, pyrrolidine dithiocarbamate (PDTC) group and PD group. Except the control group, the cells in the other three groups were exposed to hypoxia for 24 h, 30 min before which PD and PDTC were respectively added to the culture media of PDTC group and PD group, then to normoxia for 6 h. Cell survival was assessed by MTT, the protein expression of nuclear factor-κB (NF-κB) p65 was measured by immunohistochemistry, the mRNA and protein expressions of ICAM-1 were measured by RT-PCR and ELISA respectively. Results The HK2 survival cells were significantly more in PD treatment group than those in model group (P 〈 0. 05). The NF-κB p65 expressions, ICAM-1 mRNA transcriptions and protein expressions of HK2 cells, were significantly decreased in PD treatment group compared with those in control group (P 〈 0.05). There were no significant differences of the parameters mentioned above were found between the PDTC group and the PD group (P 〉 0. 05). Conolusion Polydatin has a protective effect on hypoxia/re-oxygenation induced HK2 cell injury, presumably via inhibiting the activation of NF-κB, downregulating the ICAM-1 mRNA transcription and protein expression on the surface of HK2 and finally reducing the adhesion of polymorphonuclear neutrophils.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2008年第22期2120-2123,共4页 Journal of Third Military Medical University
基金 重庆市卫生局科研基金(20042186)~~
关键词 白藜芦醇苷 缺氧复氧 HK2 核因子-ΚB 细胞间黏附分子-1 potydatin hypoxia/re-oxygenation HK2 nuclear factor-κB ICAM-1
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