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目的:探讨氨溴索对大鼠肝脏缺血再灌注损伤(I/RI)的保护作用及其机制。方法:18只雄性Wistar大鼠被随机均分为假手术组、肝I/RI模型组(模型组)、氨溴索预处理+肝I/RI模型组(氨溴索预处理组)。肝I/RI模型采用阻断入肝血流30 min后再灌注方法诱导,氨溴索预处理组于缺血前20 min尾静脉注射氨溴索(100 mg/kg),而模型组给予等体积生理盐水。术后6 h处死大鼠,检测血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)水平和肝组织病理学改变,同时检测肝组织超氧化物岐化酶(SOD),谷胱甘肽(GSH),丙二醛(MDA)含量,caspase-3的活化水平。结果:与假手术组比较,模型组与氨溴索预处理组血清ALT和AST水平明显升高(均P<0.05);肝组织出现明显的病理学改变;肝组织SOD和GSH含量明显下降,而MDA水平明显升高(均P<0.05);肝组织caspase-3活化水平明显升高(均P<0.05)。与模型组比较,氨溴索预处理组以上各项指标的变化均明显减弱(均P<0.05)。结论:氨溴索预处理能减轻大鼠肝脏I/RI,机制可能与其调控抗氧化和抗凋亡信号通路有关。
Objective: To investigate the protective effect and mechanism of ambroxol on hepatic ischemia-reperfusion injury (I / RI) in rats. Methods: Eighteen male Wistar rats were randomly divided into sham operation group, liver I / RI model group (model group), ambroxol pretreatment + liver I / RI model group (ambroxol pretreatment group). The liver I / RI model was induced by occluding the blood stream for 30 min and then reperfusion. Ambroxol preconditioning group received intravenous ambroxol (100 mg / kg) 20 min before ischemia and the model group was given Volume of normal saline. The rats were sacrificed at 6 hours after operation and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and liver histopathological changes were detected. The levels of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) content and the activation of caspase-3. Results: Compared with the sham group, the levels of ALT and AST in model group and ambroxol pretreatment group were significantly increased (all P <0.05); the pathological changes of liver tissue were observed; the contents of SOD and GSH in liver tissue were significantly decreased, (P <0.05). The activation of caspase-3 in liver tissue was significantly increased (all P <0.05). Compared with the model group, the above indexes of ambroxol pretreatment group were significantly decreased (all P <0.05). Conclusion: Ambroxol pretreatment can reduce the rat liver I / RI, the mechanism may be related to its regulation of anti-oxidation and anti-apoptotic signaling pathways.