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机构地区:[1]泸州医学院附属医院消化内科,四川泸州646000
出 处:《泸州医学院学报》2012年第3期288-290,共3页Journal of Luzhou Medical College
摘 要:目的:探讨褪黑素(melatonin,MT)在大鼠重症急性胰腺炎相关肾脏损伤发病机制中的作用。方法:90只雌性SD大鼠随机分为正常对照组、胰腺炎组、褪黑素组,各组按12、24、48h随机分配10只。采用5%牛磺胆酸钠逆行胰胆管注射的方法,复制大鼠重症急性胰腺炎相关肾脏损伤模型。用全自动生化分析仪测定大鼠血清淀粉酶,肌酐(Cr);用硫代巴比妥法测定MDA含量,黄嘌呤氧化酶法测定SOD活力;原位末端标记法(TUNEL)检测肾脏细胞凋亡率。结果:造模后各组大鼠血清淀粉酶,肌酐,MDA含量和肾脏细胞凋亡率逐渐升高,SOD活力降低;褪黑素干预后各组大鼠血清淀粉酶,肌酐,MDA含量和肾脏细胞凋亡率逐渐降低,SOD活力增加。结论:大鼠重症急性胰腺炎相关肾损伤发病过程可能与脂质过氧化引起肾脏细胞凋亡有关,褪黑素可能通过抗氧化作用对肾脏损伤起保护作用。Objective:To study the protective effect and mechanism of melatonin on renal injury related to severe acute pancreatitis. Methods: 90 female Sprague-Dawley (SD) rats were randomly divided into normal group,SAP (severe acute pancreatitis) group ,M (melatonin treatment) group. 1 mL/kg body weight of 5% sodium taurocholate was retrograde injected into the biliopancreatic duct of the rats to induce SAP. Rats in the normal group underwent operation with nothing infused.3ml melatonin solution was put to use for melation groups with subcutaneous injection.The serum amylase,creatinine(Cr),blood urea nitrogen (BUN) were measured by automatical analyzer.The MDA was measured by thiobarbituric method ,and the determination of SOD activity by xantline oxidase.Results:After the model was made,serum AMY, Cr, BUN and MDA levels of SAP groups at all time points compared with normal group were significantly higher (P〈0.01),and gradually increased with time,while SOD activity was significantly lower than normal group (P〈0.01),and gradually decreased with time.After the inter-vention of melatonin, serum AMY, Cr, BUN and MDA content of M groups compared with SAP groups at different time points were significantly lower (P〈0.01),and decreased gradually with time;while SOD activity was significantly higher than SAP groups (P〈0.01),and increased gradually with time. Conclusion:The study demonstrates that melatonin plays an protective role in SAP with acute kidney injury,the mechanism may depend on the inhibition of lipid peroxidation and reduce apoptosis in the kidney.
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