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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 investigate the protective effect of polydatin (PD) on hypoxia-reoxygenation (H/R) tubular epithelial cell injury. METHODS: Hypoxic chamber was filled with 95% N2, 5% CO2 mixed gas to simulate hypoxic environment. Human proximal proximal tubular epithelial cells (HK2) were divided into 4 groups according to different treatments: The normal control group, H/R group, PDTC group, and PD treatment group, except for the control group, were treated with hypoxia for 24 h and then treated with reoxygenation for 6 h. The cell viability was measured by MTT assay and the NF-κB p65 protein was detected by immunohistochemistry. Expression, RT-PCR detection of ICAM-1 mRNA transcription, ELISA detection of ICAM-1 protein expression. Results Compared with the H/R group, the number of HK2 cells at the corresponding time points in the PD group significantly increased (P<0.05). The positive expression of NF-κB p65 protein in the PD treatment group, the transcription of ICAM-1 mRNA and the protein expression of ICAM-1 were significantly lower than those in the control group (P<0.05). There were no statistically significant differences in the detection indexes between PD treatment group and PDTC group at each corresponding time point (P>0.05). Conclusion PD has a protective effect on H2R-induced HK2 cell injury.