论文部分内容阅读
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GSHPx)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、Fas L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/Fas L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。
Objective To investigate the effect of apigenin on the gene expression of Fas and FasL in rat renal ischemia-reperfusion injury. Methods A rat model of renal ischemia-reperfusion injury was established. Sixty rats were divided into five groups: sham operation group, ischemia reperfusion group, low concentration of apigenin group (2mg / kg), midgut concentration group / kg), high concentration of apigenin group (50mg / kg), 12 rats in each group. Serum creatinine (Cr) and blood urea nitrogen (BUN) were measured. The content of oxidative damage and antioxidation index (SOD, MDA and GSHPx) in renal tissue were determined. The pathological changes of renal tissue were observed. The expressions of FasL, caspase-3 and Bcl- 2 expression, Western blot detection of Fas, Fas L and Bcl-2 expression levels. Results Compared with the sham operation group, the levels of Cr and BUN in ischemia-reperfusion group were significantly increased; the contents of SOD and GSH-Px were significantly decreased; the content of MDA was significantly increased; the pathological tissues showed serious renal tubular injury; the expressions of FasL and caspase 3 protein expression and Bcl-2 protein expression decreased; Western blot results showed that Fas and FasL expression was significantly increased, Bcl-2 expression was significantly lower, the difference was statistically significant (P <0.01). Compared with ischemia-reperfusion group, the levels of Cr and BUN in the group of apigenin were significantly decreased; the contents of SOD and GSH-Px were significantly increased and the content of MDA was significantly decreased; the pathological tissues showed a significant improvement of renal tubule injury; the expressions of FasL, The expression of caspase-3 protein was down-regulated and the expression of Bcl-2 was up-regulated. The results of Western blot showed that the expressions of Fas and FasL were significantly decreased and the expression of Bcl-2 was significantly increased (P <0.05) . CONCLUSION: Apigenin can reduce renal ischemia-reperfusion injury and its mechanism may be related to its upregulation of Bcl-2 gene and blocking of Fas / Fas L system, thus inhibiting cell apoptosis induced by renal ischemia-reperfusion injury.