摘要
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Hoechst33258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100～500μmol／L浓度范围内处理NRK-52E细胞24h，呈浓度依赖性地增加细胞的凋亡率；500μmol／LH2O2能显著抑制NRK-52E细胞Bcl-2的表达（P〈0．05）。20μmol／L和40μmol／L姜黄素能显著阻断H202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）。40μmol／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。
Objective To explore the effect of curcumin （Cur） on oxidative stress-induced 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 Hoeehst 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 H202 treatment at the concentrations from 100 to 500μmol/L for 24 h. Expression of Bcl-2 in NRK-52E cells was obviously inhibited by exposure to 500μmol/L H2O2 （P〈0.05）. Curcumin, at concentrations of 20 μmol/L and 40μLmol/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）. Cureumin treatment alone led to an up-regulation of Bcl-2 expression （P〈0.05）. Conclusions Cureumin significantly protects NRK-52 cells against oxidative stress-induced apoptosis. The cytoproteetion may be associated with the inhibition of down-regulation of Bcl-2 expression evoked by H2O2.
出处
《中华肾脏病杂志》
CAS
CSCD
北大核心
2009年第10期761-764,共4页
Chinese Journal of Nephrology
