平胃散对湿阻中焦证AQPs损伤致水平衡失调的修复机制研究

Previous study about syndrome of accumulation of dampness in middle-jiao found that, 9 kinds of AQPs expression appeared different degrees of change in the model of rat gastrointestinal tract, and Pingwei power can influence AQPs expression. AQPs are one of the molecular foundations of maintaining the water balance. There is no influence in one study about Caenorhabditis elegans while four AQPs completely knocked, so as mammals, therefore, there must be other ways to compensate. Our team found that sodium pump activity reduced in multiple tissues of rat model, the distribution of sodium and potassium was abnormal in and out of erythrocyte, expression of intestinal GLUTs were abnormal. KCCs, NKCCs, GLUTs, SGLTs and other water transport proteins may be cooperative mode of AQPs regulation of the water balance, may be part of the essence of Pingwei power mechanism and syndrome of accumulation of dampness in middle-jiao. Because the characteristics of TCM syndrome are multiple systems and multiple targets, this project intends to research the essence of water imbalance of syndrome of accumulation of dampness in middle-jiao, through the systematic study of the distribution, content, activity, position and regulation mode of water transport proteins in gastrointestinal tract , kidney and lung, as the foundation of AQPs, combined with other water transport proteins as the starting point, with the animal mature mode of syndrome of accumulation of dampness in middle-jiao as platform, with pingwei power as the disproval. It will provide new way for the research of TCM syndromes, and provide new ideas for the development of water transport protein modulators.

湿阻中焦证前期研究发现，模型大鼠胃肠道9种AQPs表达出现不同程度改变，平胃散能影响部分AQPs表达。AQPs是维持体内水平衡的分子学基础之一。一项秀丽隐杆线虫的研究中，将四种AQPs完全敲除后表型并无影响，哺乳动物亦有此现象，因此，定有其它方式补偿。本小组发现模型大鼠多组织中钠泵活性降低，红细胞内外钠钾分布异常，肠道GLUTs表达异常。提示KCCs、NKCCs、GLUTs、SGLTs等水转运蛋白可能是AQPs调控水平衡的协同方式，可能是平胃散作用机制及湿阻中焦证的部分证本质。因中医证侯多系统、多靶点的特点，本课题拟以前期AQPs的研究为基础，结合其他水转运蛋白为切入点，以较成熟的湿阻中焦证动物模型为平台，以平胃散为反证，通过对胃肠道及肺肾水转运蛋白的分布、定量、活性、定位及调控方式的系统研究，开展湿阻中焦证水失衡证本质的研究。为中医证侯研究提供新思路，为水转运蛋白调节剂的开发提供新思路。

湿阻中焦证前期研究发现，模型大鼠胃肠道9种AQPs表达出现不同程度改变，平胃散能影响部分AQPs表达。AQPs是维持体内水平衡的分子学基础之一。一项秀丽隐杆线虫的研究中，将四种AQPs完全敲除后表型并无影响，哺乳动物亦有此现象，因此，定有其它方式补偿。本小组发现模型大鼠多组织中钠泵活性降低，红细胞内外钠钾分布异常，肠道GLUTs表达异常。提示KCCs、NKCCs、GLUTs、SGLTs等水转运蛋白可能是AQPs调控水平衡的协同方式，可能是平胃散作用机制及湿阻中焦证的部分证本质。因中医证侯多系统、多靶点的特点，本课题拟以前期AQPs的研究为基础，结合其他水转运蛋白为切入点，以较成熟的湿阻中焦证动物模型为平台，以平胃散为反证，通过对胃肠道及肺肾水转运蛋白的分布、定量、活性、定位及调控方式的系统研究，开展湿阻中焦证水失衡证本质的研究。为中医证侯研究提供新思路，为水转运蛋白调节剂的开发提供新思路。

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