姜黄素保护大鼠肾小管上皮细胞对抗氧化应激引起的损伤作用

目的 探讨姜黄素对氧化应激诱导大鼠近端肾小管上皮细胞 (NRK-52E) 损伤作用的影响。 方法 用不同浓度的H2O2处理NRK-52E细胞，建立氧化应激损伤NRK-52E的实验模型。应用Hoechst 33258染色法观察凋亡细胞的形态学改变；PI染色流式细胞仪检测细胞凋亡率；Western印迹法检测Bcl-2蛋白的表达。 结果 H2O2在100~500 μmol/L浓度范围内处理NRK-52E细胞24 h，呈浓度依赖性地增加细胞的凋亡率；500 μmol/L H2O2能显著抑制NRK-52E细胞Bcl-2的表达（P < 0.05）。20 μmol/L和40 μmol/L姜黄素能显著阻断H2O2对NRK-52E细胞的致凋亡作用（32.9±8.1）%、（22.23±9.3）%比（72.7±10.5）%，均P < 0.05]，并能显著拮抗H2O2对Bcl-2蛋白表达的下调作用（P < 0.05）。40 μmol/L姜黄素本身也能上调Bcl-2蛋白的表达（P < 0.05）。 结论 姜黄素能保护NRK-52E细胞对抗氧化应激引起的细胞凋亡，此肾小管上皮细胞保护作用可能与其抑制H2O2对Bcl-2蛋白表达的下调作用有关。

Curcumin protects NRK-52E cells against damage induced by oxidative stress

Objective To explore the effect of curcumin(Cur)on oxidative stressinduced NRK-52E cells injury.Methods NRK-52E cells were treated with H2O2 at different concentrations as an oxidative stress-induced injury model.Nucleus changes in apoptotic cells were investigated by using Hoechst 33258 staining and photofluorography.Apoptotic rate was evaluated by propidium iodide(PI)staining and flow cytometer(FCM).The expression of Bcl-2 was detected by Western blot assay.Results Apoptosis rate in NRK-52E cells was dose-dependently increased by H2O2 treatment at the concentrations from 100 to 500 μmol/L for 24 h.Expression of Bcl-2 in NRK-52E cells was obviously inhibited by exposure to 500 μmol/L H2O2(P＜0.05).Curcumin,at concentrations of 20 μmol/L and 40 μmol/L,not only decreased an elevated apoptotic rate caused by H2O2(32.9±8.1)%,(22.23±9.3)% vs(72.7±10.5)%,P＜0.05],but also blocked the inhibition of Bcl-2 expression induced by H2O2(P＜0.05).Curcumin treatment alone led to an up-regulation of Bcl-2 expression(P＜0.05).Conclusions Curcumin significantly protects NRK-52 cells against oxidative stress-induced apoptosis.The cytoprotection may be associated with the inhibition of down-regulation of Bcl-2 expression evoked by H2O2.