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目的:探讨地塞米松(DXT)对马兜铃酸(aristolochic acid,AA)诱导的人近端肾小管上皮细胞凋亡的影响及其可能机制。方法:应用不同浓度DXT处理经AA诱导的近端肾小管上皮细胞株(HK-2细胞)48h;应用Hoechst33258染色法和流式细胞技术检测HK-2细胞凋亡百分率;应用RT-PCR法测细胞Caspase-3 mRNA的表达;应用分光光度法测细胞Caspase-3酶活性。结果:40μg/mlAA可显著促进HK-2细胞凋亡,DXT可显著降低AA诱导的HK-2细胞凋亡百分率,并呈剂量依赖趋势;各组细胞Caspase-3mRNA表达水平无统计学差异;40μg/mlAA可显著升高HK-2细胞Caspase-3酶活性;而100MDXT组细胞Caspase-3酶活性较单纯40μg/mlAA刺激显著降低,而其他浓度DXT组细胞Caspase-3活性与单纯AA比较无统计学差异。结论:DXT对AA所致HK-2细胞凋亡有一定的保护作用,其机制可能是抑制细胞凋亡过程中Capease-3酶的激活。
Objective: To investigate the effect of dexamethasone (DXT) on the apoptosis of human proximal tubular epithelial cells induced by aristolochic acid (AA) and its possible mechanism. Methods: The proximal tubular epithelial cell line (HK-2) induced by AA was treated with different concentrations of DXT for 48h. The apoptosis rate of HK-2 cells was detected by Hoechst33258 staining and flow cytometry. The expression of Caspase-3 mRNA was detected by spectrophotometry. The activity of Caspase-3 was measured by spectrophotometry. Results: 40μg / ml AA could significantly promote the apoptosis of HK-2 cells. DXT could significantly reduce the percentage of apoptosis induced by AA in a dose-dependent manner. There was no significant difference in the expression of Caspase-3 mRNA in 40μg / ml AA / ml AA significantly increased Caspase-3 activity in HK-2 cells; Caspase-3 activity was significantly decreased in 100MDXT cells compared with 40μg / ml AA alone, but no significant difference was found between other concentrations of DXT and AA Differences CONCLUSION: DXT can protect HK-2 cells from apoptosis induced by AA, which may be due to the inhibition of the activation of Capease-3 during apoptosis.