功能性腹泻脾虚证模型大鼠肠组织钠离子通道蛋白的变化  

Changes of sodium channel protein in intestine of functional diarrhea model rats with spleen deficiency

作　　者：李家立[1] 王亮[2] 白艳香 季庆洁[2] 康楠[1] LI Jiali;WANG Liang;BAI Yanxiang;JI Qingjie;KANG Nan(Department of Traditional Chinese Medicine,Affiliated Hospital of Ji′ning Medical University,Shandong Province,Ji′ning 272029,China;Department of Adult Rehabilitation,Affiliated Hospital of Ji′ning Medical University,Shandong Province,Ji′ning 272029,China;Department of Clinical Laboratory,Affiliated Hospital of Ji′ning Medical University,Shandong Province,Ji′ning 272029,China)

机构地区：[1]济宁医学院附属医院中医科,山东济宁272029 [2]济宁医学院附属医院成人康复科,山东济宁272029 [3]济宁医学院附属医院检验科,山东济宁272029

出　　处：《中国医药导报》2020年第16期8-10,15,共4页China Medical Herald

基　　金：国家自然科学基金青年科学基金项目(81804064);山东省自然科学博士基金项目(ZR2018BH034)。

摘　　要：目的观察功能性腹泻脾虚证模型大鼠肠组织NHE3、Na+-K+-ATPase、ENaC等离子通道蛋白的表达变化。方法采用随机数字表法将24只3周龄雄性Wistar大鼠分为正常组和模型组,利用小平台站立法联合高乳糖饲料喂养建立功能性腹泻脾虚证模型,造模14 d后取材,采用Western blot检测肠组织中的各指标蛋白表达变化。结果造模后1 d,两组大鼠体重均显著重于造模前1 d(P<0.01),但模型组显著轻于正常组(P<0.01)。模型组大鼠腹泻率为100%。造模后,模型组大鼠结肠NHE3、Na+-K+-ATPase相对表达量均低于正常组(P<0.05或P<0.01),NHERF2、PKAR2相对表达量均高于正常组(P<0.05或P<0.01)。结论Na+-K+-ATPase、NHE3等Na+通道蛋白的表达下调可能是功能性腹泻脾虚证发生的分子生物学基础,值得进一步研究证实。Objective To observe the changes of NHE3,Na+-K+-ATPase and ENaC in intestine of functional diarrhea model rats with spleen deficiency.Methods Twenty-four male Wistar rats(3 weeks old)were divided into normal group and model group according to the random number table method.The model rats of functional diarrhea with spleen deficiency syndrome were made using the modified multiple platform method and high lactose feed.After the model was made,the materials were taken and the expression of various indexes in intestinal tissue was detected by Western blot.Results The first day after molding,the weight of rats in both groups was significantly heavier than that in the first day before modeling(P<0.01),but the weight of rats in model group was significantly lighter than that in normal group(P<0.01).The diarrhea rate of rats in model group was 100%.After molding,the relative expression of NHE3 and Na+-K+-ATPase in colon of model group was lower than that of normal group(P<0.05 or P<0.01),the relative expression of NHERF2 and PKAR2 in colon of model group was higher than that of normal group(P<0.05 or P<0.01).Conclusion The down-regulation of Na+-K+-ATPase,NHE3 and other sodium channel proteins may be the molecular biological basis of spleen deficiency syndrome of functional diarrhea,which is worth further study and confirmation.

关 键 词：腹泻 脾虚 Na+通道 NHE3 Na+-K+-ATPase 

分 类 号：R-332[医药卫生]