中文摘要：

目的：建立湿阻中焦证Cajal间质细胞模型并对其进行评价。方法：湿阻中焦证动物模型建立及动物血清制备;采用Ⅱ胶原酶消化法体外培养ICC,通过湿阻中焦证动物模型含药血清建立体外湿阻中焦证Cajal间质细胞模型,模拟湿阻中焦证大鼠模型体内ICC的生长,以及平胃散含药血清在湿阻中焦证治疗中对ICC细胞的调节机制,反证证候细胞模型建立成功。结果：细胞造模后细胞内Na^＋-K^＋-ATP酶（Na^＋-K^＋-Atpase）活力下降,K^＋浓度及ATP升高,ICC细胞无氧代谢能力增强;湿阻中焦证细胞经平胃散血清干预后,与自然恢复组比较平胃散组ICC细胞Na^＋-K^＋-Atpase和K＋活性升高明显、ATP下降、LDH活力降低。结论：湿阻中焦证ICC模型细胞与正常ICC存在差异,证侯细胞模型建立成功;钠钾泵活性的改变可能是湿阻中焦证的基本病理改变之一,平胃散可能通过恢复钠钾泵活性阻断K^＋浓度的下降趋势,影响中焦湿阻证Cajal间质细胞代谢。

英文摘要：

Objective： Establishement and evaluature of of interstitial cells of Cajal spleen and stromach bloked by dampness syndrone in vitro study. Methods： The dampness obstructing spleen stomach syndrome animal model establishment and animal serum preparation; ICC cultured in vitro by collagenase ]I , The dampness containing animal serum in vitro model of middle energizer dampness obstructing spleen stomach syndrome of interstitial cells of Cajal model, Simulation of rat model in vivo ICC growth,Pingwei power and serum regulating mechanism of ICC cells in the treatment of dampness syndrome. The successful establishment of cell model counterevidence syndrome. Results- After the cell model was made, the Na ~ -K ＋ -ATP enzyme activity decreased, K ~ concentration and ATP increased, and the anaerobic metabolism ability of ICC cells was enhanced. Wet resistance of middle energizer cells through a fiat stomach scattered serum intervention, and natural recovery group compared, fiat stomach scattered group ICC Na ＋ -K ＋ -ATPase and K activity was significantly increased, the decline in ATP and LDH activity decreased. Conclusion：The dampness obstructing spleen stomach syndrome ICC model cells and normal ICC have differences. The successful cell model was established successfully, the sodium pump activity is the basic pathological change in the change of the dampness obstructing spleen stomach syndrome, and the level of the stomach may be through the recovery of sodium potassium pump activity, Blocking the downward trend of K ＋ concentration of dampness obstructing spleen stomach syndrome in the Cajal interstitial cell metabolism.