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| Changes of sodium channel protein in intestine of functional diarrhea model rats with spleen deficiency |
| LI Jiali1 WANG Liang2 BAI Yanxiang3 JI Qingjie2 KANG Nan1 |
1.Department of Traditional Chinese Medicine, Affiliated Hospital of Ji′ning Medical University, Shandong Province, Ji′ning 272029, China;
2.Department of Adult Rehabilitation, Affiliated Hospital of Ji′ning Medical University, Shandong Province, Ji′ning 272029, China;
3.Department of Clinical Laboratory, Affiliated Hospital of Ji′ning Medical University, Shandong Province, Ji′ning 272029, China |
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Abstract 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.
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