【摘要】 背景:肾脏缺血再灌注常合并肾脏及肺脏的急性损伤,且角质细胞生长因子受体及钠通道蛋白在缺血再灌注致急性肾、肺损伤中的表达变化及α-促黑素的治疗作用有待于进一步观察及研究。目的:探索全肾缺血再灌注模型大鼠中角质细胞生长因子受体、钠通道蛋白的表达以及α-促黑素的治疗作用。方法:选择健康雄性SD大鼠30只按随机数字表法等分为对照组、缺血再灌注造模组和α-促黑素干预组。缺血再灌注造模组和α-促黑素组大鼠通过肾动脉结扎30 min建立全肾缺血/再灌注模型,对照组大鼠仅暴露肾动脉不结扎。α-促黑素干预组大鼠于造模前30 min腹腔注射α-促黑素(0.25 mg/kg)进行干预,缺血再灌注造模组大鼠注射等量(4 mL)生理盐水。结果与结论:与对照组相比,缺血再灌注造模组与α-促黑素干预组大鼠肾、肺组织含水量明显升高,角质细胞生长因子受体、钠通道蛋白的表达明显下降(P<0.05);与缺血再灌注造模组相比,α-促黑素干预组大鼠肾、肺组织含水量明显减少,而角质细胞生长因子受体、钠通道蛋白mR NA及蛋白的表达明显升高(P<0.05),且大鼠肾、肺组织充血水肿明显减轻。提示肾缺血再灌注后,角质细胞生长因子受体、钠通道蛋白的表达变化与肾、肺充血水肿等损伤一致,而α-促黑素可以增加角质细胞生长因子受体、钠通道蛋白的表达水平,减轻肾及肺组织的损伤,发挥一定的保护作用。更多还原

【Abstract】 BACKGROUND: Kidney ischemia-reperfusion injury often combines with acute kidney and lung injury. The expression of cutin cell growth factor receptor(KGFR) and alpha sodium channel protein(α-ENa C) in kidney and lung after ischemia-reperfusion injury and the protective effect of α-melanocyte require further observation and research. OBJECTIVE: To explore the therapeutic effect of α-melanocyte on the expressions of KGFR and α-ENa C in rat models of ischemia-reperfusion injury. METHODS: A total of 30 healthy male Sprague-Dawley rats were randomly divided into control group, ischemia-reperfusion group and α-MSH group. Models of renal ischemia-reperfusion injury were established by 30-minute ligation of renal artery in the ischemia-reperfusion and α-melanocyte groups. Rats in the control group were only used to expose the renal artery, no ligation. Rats in the α-melanocyte group were intraperitoneally injected with α-melanocyte(0.25 mg/kg) at 30 minutes before model establishment. Rats in the ischemia-reperfusion group were injected with 4 m L of physiological saline. RESULTS AND CONCLUSION: Compared with control group, water content of kidney and lung increased significantly in rats of ischemia-reperfusion group and a-MSH group, while the levels of KGFR and α-ENa C of kidney and lung in rats were lower(P < 0.05). Compared with the ischemia-reperfusion group, water content of kidney and lung in rats of a-MSH group decreased significantly, while the levels of KGFR and α-ENa C of kidney and lung increased gradually(P < 0.05). Moreover, edema was significantly lessened in the rat kidney and lung. Results confirmed that after renal ischemia-reperfusion injury, KGFR and α-ENa C expression was consistent to the kidney and lung injury. α-MSH could increase the protein and m RNA expression of KGFR and α-ENa C in kidney and lung of rats, reduce the kidney and lung injury, and exert a certain protective effect.更多还原