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脾气虚大鼠小肠组织Ca^(2+)/CaM信号通路关键分子的表达变化     被引量:3

Expression changes of key molecules of Ca^(2+)/CaM signaling pathway in small intestine tissue of rats with syndrome of deficiency of spleen qi

文献类型:期刊文献

中文题名:脾气虚大鼠小肠组织Ca^(2+)/CaM信号通路关键分子的表达变化

英文题名:Expression changes of key molecules of Ca^(2+)/CaM signaling pathway in small intestine tissue of rats with syndrome of deficiency of spleen qi

作者:成映霞[1,2];杜娟[1];杨晓轶[1,2];段永强[2,3];程卫东[3];梁玉杰[1,2];李兰珍[1];高建德[1];安耀荣[1];王燕[1]

第一作者:成映霞

机构:[1]甘肃中医药大学;[2]甘肃中医药大学甘肃省中药新产品创制重点实验室;[3]兰州大学基础医学院中西医结合研究所

第一机构:甘肃中医药大学

年份:2015

卷号:30

期号:10

起止页码:3624

中文期刊名:中华中医药杂志

外文期刊名:China Journal of Traditional Chinese Medicine and Pharmacy

收录:CSTPCD;;北大核心:【北大核心2014】;CSCD:【CSCD_E2015_2016】;

基金:国家自然科学基金项目(No.81160420);甘肃省自然科学基金项目(No.1010RJZA148);甘肃省教育厅基金项目(No.1006-05)~~

语种:中文

中文关键词:脾气虚证;Ca2+/CaM信号通路;小肠;大鼠

外文关键词:Syndrome of deficiency of spleen qi; Ca(2+)/CaM signaling pathway; Small intestine; Rats

摘要:目的:观察脾气虚大鼠小肠组织Ca2+/Ca M信号通路中关键分子[Ca2+]i浓度以及Ca M、Ca MKⅡ、p-Ca MKⅡ蛋白表达水平的变化。方法:受试动物随机分为4组,即空白对照组,脾虚模型7d、14d、21d组,每组12只。除空白对照组外,其余受试动物采用复合法(苦寒破气法、游泳力竭法及饥饱失常法)成功建立脾气虚证大鼠模型,在观测各组大鼠一般生存状态、胃肠转运功能和小肠组织能量代谢相关酶活性的基础上,采用激光共聚焦技术检测小肠组织细胞内[Ca2+]i浓度,蛋白免疫印迹技术检测小肠组织Ca M、Ca MKⅡ和p-Ca MKⅡ的表达变化。结果:与空白对照组比较,脾气虚大鼠随着造模时间的延长,胃残留率升高而小肠推进率下降(P<0.01);小肠组织乳酸脱氢酶(LDH)活性升高而琥珀酸脱氢酶(SDH)活性降低(P<0.05,P<0.01);小肠组织[Ca2+]i浓度和Ca M、Ca MKⅡ、p-Ca MKⅡ蛋白表达量显著升高(P<0.01);且脾虚模型7d、14d、21d组之间比较,以脾虚模型21d组变化更为显著(P<0.05,P<0.01)。结论:小肠组织Ca2+/Ca M信号通路关键分子的异常表达变化可能是脾气虚发生的病理机制之一。
Objective:To observe the changes in expression of the key molecules as CaM,CaMKII and p-CaMKⅡof Ca^(2+)/CaM signaling pathways in small intestine tissue of rats with syndrome of deficiency of spleen qi.Methods:Rats were randomly divided into 4 groups as control group,7d,14 d and 21 d model groups,and with 12 rats in each group.All the rats except rats in control group were used to establish the rat models with syndrome of deficiency of spleen qi by using a compound method,which included method of bitter-cold and removing stagnant qi,method of exhausting by swimming and method of either hunger or gorge.To test the concentration of[Ca^(2+)]i in small intestine tissue by using laser confocal microscopy based on the observation of general condition,gastrointestinal transshipment function and activity of enzymes related with energy metabolism in small intestine of rats.The changes in expression of proteins as CaM,CaMKⅡ,p-CaMKⅡ in small intestine were tested by using Western blot method.Results:Compared with control group,the stomach residue rate of rats with syndrome of deficiency of spleen qi was increased,and the small intestine propelling rate of rats in model groups was decreased with the prolongation of model establishing time(P〈0.01).The activity of LDH in small intestine of rats in model groups was increased,and the activity of SDH was decreased(P〈0.05,P〈0.01).The concentration of[Ca^(2+)]i and the expression of CaM,CaMKⅡ and p-CaMKⅡ in small intestine tissue of rats in model groups were increased significantly(P〈0.01),and these changes in rats of 21 d model group were the most remarkable compared with rats in 7d and 14 d model groups(P〈0.05,P〈0.01).Conclusion:The abnormal expression of the key molecules of Ca^(2+)/CaM signaling pathways in small intestine tissue might be one of the pathogenic mechanisms in the occurrence of syndrome of deficiency of spleen qi.

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