NAC对缺氧复氧后肾小管上皮细胞凋亡的干预作用

The Study of Apoptosis of HK2 and Effect of NAC on Renal Tubular Epithelial Cells with Hypoxia Reoxygenation

目的:研究缺氧复氧后肾小管上皮细胞凋亡的表达及N-乙酰半胱胺酸(NAC)对其的影响。方法:选用人肾小管上皮细胞(HK2)建立缺氧复氧损伤模型,设正常对照组、单纯缺氧复氧组、不同浓度(1mmol/L、5mmol/L、10mmol/L)NAC干预组。流式细胞术检测细胞内氧化应激水平与细胞凋亡表达。结果:缺氧复氧后HK2细胞内氧化应激水平提高,HK2细胞凋亡细胞和死亡细胞数量增多,且随缺氧时间的延长,细胞内氧化应激水平逐渐升高,凋亡细胞和死亡细胞数量逐渐增多;NAC呈剂量关系抑制细胞内氧化应激水平,同时呈剂量关系减少凋亡细胞和坏死细胞的数量。结论:缺氧复氧诱导细胞内氧化应激的产生,诱导HK2细胞凋亡和死亡;NAC可以通过抑制细胞内氧化应激减少细胞和坏死细胞的数量。

Objective：To investigate the mechanism of apoptosis of renal tubular epithelial cells with hypoxia reoxygenation （H/R）and to evaluate the effects of NAC on it. Methods：The cutueled renal epithelial cells（HK2） were divided into groups：normal control group,H/R group, 1 mM NAC＋ H/R group,5 mM NAC＋ H/R group, 10 mM NAC＋ H/R group. The flow cytometry was used to detect the oxidative. The flow cytometry was used to detect the apoptosis of HK2 Result The oxidative stress in HK2 was induced after H/R. The amounts of apoptosis and necrosis of HK2 were increasd after H/R. Results： stress in HK2 was inhibited by NAC with a dose- dependent manner. The apoptosis and death of HK2 cells were inhibited by NAC with a dose - dependent manner. Conclusion： H/R injury the HK2 cells by oxidative stress and induce apoptosis and necrosis of HK2. NAC protected HK2 cells against H/R injury by inhibiting oxidation.