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目的:探讨辛伐他汀对肾缺血再灌注损伤(IRI)的影响及其作用机制。方法:30只雄性SD大鼠分成3组,治疗组术前连续3 d给予辛伐他汀10 mg·kg-1·d-1 ig,模型组和假手术组术前3 d生理盐水ig。治疗组与模型组大鼠左肾肾蒂夹闭45 min以诱导缺血再灌注损伤,并将右肾切除。假手术组仅行右肾切除术。术前和术后24 h取血;术后24 h处死大鼠,检测血清肌酐水平,了解肾脏功能及受损情况,观察肾组织病理改变,运用蛋白免疫印迹方法检测血红素氧合酶-1(HO-1)的表达水平,运用免疫组化方法对HO-1和ED-1阳性巨噬细胞进行定位。结果:治疗组和模型组相比,血清肌酐水平、肾损伤明显降低(P<0.05),肾组织中HO-1表达明显增加(P<0.05),表达HO-1的大部来自浸润的单核/巨噬细胞。结论:辛伐他汀能正向调节肾组织中HO-1的表达,从而发挥其抗炎作用,减轻肾组织损伤。
Objective: To investigate the effect of simvastatin on renal ischemia-reperfusion injury (IRI) and its mechanism. Methods: Thirty male Sprague-Dawley rats were divided into three groups. Simvastatin 10 mg · kg-1 · d-1 ig was given to the treatment group 3 days before operation, and normal saline ig was given to the model group and sham operation group three days before operation. The left renal pedicle of rats in the treatment group and the model group were occluded for 45 min to induce ischemia-reperfusion injury, and the right kidney was excised. Sham operation group only right nephrectomy. The blood samples were collected 24 h after operation and sacrificed 24 h after operation. Serum creatinine level was measured and renal function and damage were observed. The pathological changes of renal tissues were observed. The levels of heme oxygenase-1 HO-1 and ED-1 positive macrophages were detected by immunohistochemistry. Results: Compared with model group, serum creatinine level and renal injury were significantly decreased in treatment group (P <0.05), and HO-1 expression in renal tissue was significantly increased (P <0.05). Most of the expression of HO-1 was from single infiltration Nuclear / macrophages. Conclusion: Simvastatin can positively regulate the expression of HO-1 in renal tissues, thus exerting its anti-inflammatory effect and reducing renal tissue injury.