芹黄素对肾缺血再灌注损伤后Fas/FasL介导凋亡反应的影响

目的 探讨芹黄素抑制大鼠肾缺血再灌注损伤凋亡Fas、FasL基因表达的影响。方法 建立大鼠肾缺血再灌注损伤模型，将60只大鼠分为5组：假手术组、缺血再灌注组、芹黄素低浓度组（2mg/kg）、芹黄素中浓度组（10mg/kg）、芹黄素高浓度组（50mg/kg），每组大鼠各12只。检测血清肌酐（Cr）和尿素氮（BUN），测定肾组织氧化损伤和抗氧化指标（SOD、MDA和GSH-Px）含量，观察肾组织病理学变化，免疫组化检测FasL、caspase-3和Bcl-2表达，Western blot法检测Fas、FasL和Bcl-2表达水平。结果 与假手术组比较，缺血再灌注组Cr和BUN水平均明显增高；SOD和GSH-Px含量明显降低，MDA含量显著升高；病理组织显示肾小管损伤严重；免疫组化示FasL、caspase-3蛋白表达增强，Bcl-2表达降低；Western blot法检测结果显示Fas和FasL表达水平明显升高，Bcl-2表达水平明显降低，差异有统计学意义（P<0.01）。与缺血再灌注组比较，芹黄素组Cr和BUN水平均明显降低；SOD和GSH-Px含量明显升高，MDA含量显著下降；病理组织显示肾小管损伤显著改善；免疫组化显示FasL、caspase-3蛋白表达较表达下调，Bcl-2表达上调；Western blot法检测结果显示，Fas和FasL和表达水平明显下降，Bcl-2表达水平明显升高，差异有统计学意义（P<0.05）。结论 芹黄素能减轻肾脏缺血再灌注损伤，其机制可能与其上调Bcl-2基因和阻断Fas/FasL系统有关，从而抑制肾缺血再灌注损伤后所造成的细胞凋亡。

Effects of Apigenin on Renal Ischemia/reperfusion Injury Apoptosis in Rats by Fas/FasL

Objective To investigate the effect of apigenin and the change of expression of Fas/FasL after renal ischemia/reperfusion injury in rats. Methods Establishing Renal ischemia/reperfusion injury rat model was established. Sixty rats were randomly divided into 5 Groups. Blood samples were collected for the detection of serum creatinine and urea nitrogen levels. The level of SOD,MDA and GSH-Px were detected. Histologic examinations were evaluated. The expression of Fas, FasL, Caspase-3 and Bcl-2 were performed by immunohistochemistry and Western blot. Results Compared with the sham group, the Cr and BUN levels in the I/R groups of were significantly increased, the level of SOD and GSH-Px reduced, the level of MDA improved. Histopathological damage of renal tubular aggravated. The immunohistochemical expression of FasL and Caspase-3 as shown in enhanced and Bcl-2 reduced. Western blot showed that Fas and FasL expression increased and Bcl-2 reduced significantly, and the difference was statistically significant(P<0.05). Compared with I/R group, apigenin significantly enhanced renal function, and alleviated renal tubular epithelial cell injury and decreased Fas, FasL and Caspase-3 expression, improved Bcl-2 expression, difference were statistically significant(P<0.05). Conclusion Apigenin can protect the rats subjected to ischemia/reperfusion injury. Its protective mechanism may be related to the inhibition in expression of Fas/FasL and the increase in expression of Bcl-2.