氨溴索对大鼠肝脏缺血再灌注损伤的保护作用

发布时间：2018-05-26 22:09

本文选题：再灌注损伤 + 肝　；参考：《中国普通外科杂志》2013年01期

【摘要】：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P0.05);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P0.05);肝组织caspase-3活化水平明显升高(均P0.05)。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P0.05)。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。
[Abstract]:Aim: to investigate the protective effect and mechanism of ambroxol on hepatic ischemia reperfusion injury (I / R) in rats. Methods 18 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 preconditioning group). The hepatic I/RI model was induced by reperfusion after 30 min occlusion of hepatic blood flow. The ambroxol preconditioning group was injected with ambroxol 100 mg 路kg ~ (-1) 路kg ~ (-1) by tail vein 20 min before ischemia, while the model group was given the same volume of normal saline. The rats were killed 6 hours after operation. The levels of serum alanine aminotransferase (alt) and aspartate aminotransferase (AST) and the pathological changes of liver tissue were detected. The contents of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and the activation of caspase-3 were also detected. Results: compared with sham operation group, serum ALT and AST levels in model group and ambroxol preconditioning group were significantly increased (P0.05A, P < 0.05). The pathological changes were observed in liver tissue, and the contents of SOD and GSH in liver tissue decreased significantly. However, the level of MDA was significantly increased (P 0.05) and the level of caspase-3 activation in liver tissue was significantly increased (P 0.05). Compared with the model group, the changes of the above indexes in ambroxol pretreatment group were significantly decreased (P 0.05). Conclusion: ambroxol preconditioning can attenuate I / R in rat liver, and the mechanism may be related to its regulation of antioxidant and anti-apoptotic signaling pathways.
【作者单位】：哈尔滨医科大学附属五院普通外科;哈尔滨医科大学大庆校区基础医学系;
【基金】：黑龙江省自然科学基金资助项目(D200927)
【分类号】：R363

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