论文部分内容阅读
目的:观察脾气虚大鼠小肠组织钙调蛋白信号通路中钙调蛋白(Ca M)、钙调素依赖蛋白激酶Ⅱ(Ca MKⅡ)基因表达规律,揭示脾气虚证发生的内在机制。方法 :将48只大鼠随机分为正常对照组和脾气虚7 d、14 d、21 d组4组,每组12只。除正常对照组外,其余各组采用复合法(苦寒破气法、力竭法及饥饱失常法)建立脾气虚证大鼠模型,观测各组大鼠一般生存状态、脾虚证宏观证候积分、平均每日体质量增加量、负重游泳耐力时间和基础肛温;同时,采用实时荧光定量PCR技术检测小肠组织钙调蛋白信号通路中Ca M、Ca MKⅡ基因表达水平的变化。结果:与正常对照组对比,脾气虚模型7 d、14 d、21 d组大鼠平均每日体质量增加量、负重游泳耐力和基础肛温降低,脾虚证宏观证候积分升高,小肠组织Ca M、Ca MKⅡ基因相对表达量显著升高,且以脾气虚模型21 d组变化显著(P<0.05)。结论:脾气虚大鼠小肠组织钙调蛋白信号通路中Ca M、Ca MKⅡ基因表达水平异常增高。
Objective: To observe the expression of calmodulin (Ca M) and calmodulin dependent protein kinase Ⅱ (Ca MK Ⅱ) in the small intestinal tissue of spleen deficiency rats, and to reveal the underlying mechanism of the spleen qi deficiency syndrome. Methods: Forty-eight rats were randomly divided into normal control group and spleen-qi deficiency group for 7 d, 14 d and 21 d groups, with 12 rats in each group. In addition to the normal control group, the remaining groups using the compound method (bitter cold and dampness method, exhaustion method and hungry method) to establish the rat model of spleen deficiency syndrome, observed the general survival of rats in each group, the spleen deficiency syndrome macro syndromes score , Mean daily body mass gain, swimming time and basic rectal temperature. At the same time, real-time fluorescent quantitative PCR was used to detect the changes of Ca M and Ca MKⅡ gene expression in the small intestinal tissue calmodulin signaling pathway. Results: Compared with the normal control group, the mean daily body mass gain, weight-bearing swimming endurance and basal rectal temperature in the spleen-qi deficiency model group on the 7th, 14th and 21st days were significantly decreased, while the macro syndrome scores in the spleen deficiency syndrome were increased. Ca M, Ca MKⅡ gene relative expression was significantly increased, and the spleen deficiency model 21 d group changes significantly (P <0.05). Conclusion: CaM, Ca MKⅡ gene expression in calmodulin signaling pathway of spleen deficiency rats is abnormally increased.