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目的 探讨低氧在肾脏疾病进展中的作用机制。方法 将肾小管上皮细胞MDCK分别置于低氧3％和正常氧18％条件下,培养24,48,72和96 h。应用台盼蓝排除法计数活细胞,观察细胞增殖;应用流式细胞仪观察细胞周期;以及半定量RT-PCR检测MDCK细胞TGF-β1mRNA的表达。结果 低氧可促进MDCK细胞增殖,G0-G1期细胞比例减少,G2-M期细胞比例增多。低氧可促进TGF-β1 mRNA的表达,而且呈一定时间相关性。结论 慢性低氧致肾间质纤维化的机制与低氧引起的细胞增殖和细胞周期的改变有关,而这些改变又可能与低氧引起的细胞分泌生长因子改变有关。
Objective To investigate the mechanism of hypoxia in the progression of renal disease. Methods The renal tubular epithelial cells (MDCKs) were exposed to 3% hypoxia and 18% normal oxygen for 24, 48, 72 and 96 h, respectively. The viable cells were counted by trypan blue exclusion method and the cell proliferation was observed. The cell cycle was observed by flow cytometry. The expression of TGF-β1 mRNA in MDCK cells was detected by semi-quantitative RT-PCR. Results Hypoxia could promote the proliferation of MDCK cells, the proportion of cells in G0-G1 phase decreased, and the proportion of G2-M phase cells increased. Hypoxia can promote the expression of TGF-β1 mRNA, but also a certain time correlation. Conclusion The mechanism of chronic hypoxia-induced interstitial fibrosis is related to hypoxia-induced cell proliferation and cell cycle changes, which may be related to the changes of cell growth factors induced by hypoxia.