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作 者:蔡治方[1] 彭慈军[1] 兑丹华[1] 傲宇 兰天罡[1] CAI Zhifang;PENG Cijun;DUI Danhua;AO Yu;LAN Tiangang(Department of Hepatobiliary Surgery,the Affiliated Hospital,Zunyi Medical College,Zunyi,Guizhou 563000)
机构地区:[1]遵义医学院附属医院肝胆外科
出 处:《郑州大学学报(医学版)》2019年第5期754-757,共4页Journal of Zhengzhou University(Medical Sciences)
基 金:贵州省科技计划项目(黔科合LH字[2016]7478)
摘 要:目的:探讨清胰Ⅱ号对急性胰腺炎大鼠的保护作用及其可能的作用机制。方法:36只SD大鼠均分为正常组、模型组、治疗组。手术联合注射牛磺胆酸钠制备急性胰腺炎大鼠模型,术后正常组与模型组用生理盐水灌胃,治疗组用250 g/L清胰Ⅱ号按10 mL/kg灌胃,6 h一次。于第4次灌胃后处死大鼠收集胰腺、肠组织以及血液。胰腺组织HE染色后观察病理变化;采用ELISA法检测大鼠血浆淀粉酶及血浆中IL-6、MCP-1含量;采用双氢罗丹明-123法检测大鼠胰腺组织中ROS,氧化酶反应法检测大鼠胰腺组织中SOD,钼酸铵终止法检测CAT,硫代巴比妥酸法检测MDA;细菌培养法检测大鼠肠道细菌数量以及分类;Western blot法检测大鼠胰腺组织中JNK蛋白的表达。结果:模型组与正常组比较,组织病理学评分、血浆淀粉酶活性、IL-6、MCP-1、ROS、MDA、肠道细菌数、JNK蛋白表达水平均升高,SOD、CAT降低(P<0.05);治疗组与模型组比较,胰腺组织病理学评分、血浆淀粉酶活性、IL-6、MCP-1、ROS、MDA、肠道细菌数、JNK蛋白表达水平降低,SOD、CAT升高(P<0.05)。结论:清胰Ⅱ号对急性胰腺炎大鼠具有保护作用,其机制可能与抑制ROS/JNK通路有关。Aim:To investigate the protective effect of QingyiⅡon acute pancreatitis rats and its related mechanism.Methods:Thirty-six SD rats were randomly allocated into normal group,model group and treatment group(12 in each group).Rat models of acute pancreatitis were prepared by injection of sodium taurocholate.Rats in the normal group and the model group were intragastrically administered with normal saline,and the treatment group was given 250 g/L QingyiⅡat 10 mL/kg every 6 hours.After the fourth intragastric administration,the rats were killed to collect pancreas,intestines and blood.The pathological changes of pancreatic tissue were observed after HE staining.ELISA was used to detect the plasma amylase activity and the contents of IL-6 and MCP-1 in plasma.ROS in the pancreas was detected by the method of double-hydrogen rhodamine-123.SOD in the pancreas of rats was detected by oxidase reaction.CAT and MDA were detected by ammonium molybdate colorimetry and thiobarbituric acid method.The number and classification of intestinal bacteria in rats were detected by bacterial culture.The JNK protein in the pancreatic tissue of rats was detected by Western blot.Results:Compared with normal group,histopathological score,plasma amylase activity,IL-6,MCP-1,ROS,MDA,intestinal bacteria count,and JNK protein expression level in the model group increased,while the levels of SOD and CAT decreased(P<0.05).Compared with the model group,the pathological score of pancreas,plasma amylase activity,IL-6,MCP-1,ROS,MDA,intestinal bacterial count and JNK protein expression level in the treatment group decreased,while the levels of SOD and CAT increased(P<0.05).Conclusion:QingyiⅡhas obvious protective effects on acute pancreatitis model rats,and its mechanism may be related to inhibition of ROS/JNK pathway.
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