Rosuvastatin reduces rat intestinal ischemia-reperfusion injury associated with the preservation of endothelial nitric oxide synthase protein

瞄准：为了在 ischemia-reperfusion (红外) 上调查 rosuvastatin 的保护的效果，并且在内皮的氮的氧化物 synthase (eNOS ) 的表示上决定这个代理人的效果，在老鼠导致了小肠的损害和发炎蛋白质。方法：肠的损坏被为 30 min 夹钳优异 mes 伤寒动脉和腹的箱子在男 Sprague-Dawley 老鼠导致，为 60 min 由灌注列在后面。在生理盐水溶解的 Rosuvastatin intraperitoneally 被管理在局部缺血前的 60 min。肠的粘膜损害和发炎的严厉被几个生物化学的标记，以及由组织检查所见评估。eNOS 的蛋白质层次被西方的污点决定。结果：当粘膜的索引损坏，管腔内血红素和蛋白质的层次显著地在假冒操作组与那些相比在红外组被增加。然而，这些增加被处理显著地以一种剂量依赖者方式与 rosuvastatin 禁止。rosuvastatin 的保护的效果被组织检查所见也证实。到红外的小肠的暴露导致了 thiobarbituric 的重要增加描绘的粘膜发炎酸反应的物质，联系织物的 myeloperoxidase 活动，和老鼠的粘膜内容导致 cytokine 的嗜中性的 chemoattractant-1 (CINC-1 ) 和肿瘤坏死 factor-alpha (TNF-alpha ) 。在红外以后的煽动性的参数的这些增加被预告的处理显著地在 10 mg/kg 的剂量与 rosuvastatin 禁止。而且， CINC-1 和 TNF-alpha 的 mRNA 表示在红外以后被增加，并且这增加被 rosuvastatin 也禁止。eNOS 的粘膜蛋白质层次在红外期间减少了，但是在与 rosuvastatin 对待的老鼠被保存。结论：Rosuvastatin 禁止老鼠红外导致的肠的损害和发炎，和它的保护与 eNOS 的保藏被联系蛋白质。

AIM： To investigate the protective effect of rosuvastatin on ischemia-reperfusion （I-R）-induced small intestinal injury and inflammation in rats, and to determine the effect of this agent on the expression of endothelial nitric oxide synthase （eNOS） protein. METHODS： Intestinal damage was induced in male Sprague-Dawley rats by clamping both the superior mesenteric artery and the celiac trunk for 30 min, followed by reperfusion for 60 min. Rosuvastatin dissolved in physiological saline was administered intraperitoneally 60 min before ischemia. The severity of the intestinal mucosal injury and inflammation were evaluated by several biochemical markers, as well as by histological findings. The protein levels of eNOS were determined by Western blot. RESULTS： The levels of both intraluminal hemoglobin and protein, as indices of mucosal damage, were significantly increased in the I-R group compared with those in the sham-operated group. These increases, however, were significantly inhibited by treatment with rosuvastatin in a dose-dependent manner. The protective effects of rosuvastatin were also confirmed by histological findings. Exposure of the small intestine to I-R resulted in mucosal inflammation characterized by significant increases in thiobarbituric acid-reactive substances, tissueassociated myeloperoxidase activity, and the mucosal contents of rat cytokine-induced neutrophil chemoattracrant-1 （CINC-1） and tumor necrosis factor-α（TNF-α）. These increases in inflammatory parameters after I-R were significantly inhibited by pretreatment with rosuvo astatin at a dose of 10 mg/kg. Furthermore, mRNA expression of CINC-1 and TNF-α was increased after I-R, and this increase was also inhibited by rosuvastatin. The mucosal protein levels of eNOS decreased during I-R, but were preserved in rats treated with rosuvastatin. CONCLUSION： Rosuvastatin inhibits rat intestinal injury and inflammation induced by I-R, and its protection is associated with the preservation of eNOS protein.