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目的探讨脾气虚大鼠骨骼肌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(Ca MK)Ⅱ基因表达变化规律。方法受试动物随机分为空白组、脾气虚模型组(7 d、14 d、21 d组),每组10只。除空白组外,其余受试动物采用复合法(苦寒破气法、力竭法及饥饮失常法)成功建立脾气虚证大鼠模型后,在观察各组大鼠一般生存状态、脾虚证宏观证候积分、平均每日摄食量、平均每日体重增加量和负重游泳耐力的同时,采用实时荧光定量PCR技术检测骨骼肌组织Ca M信号通路中Ca M、Ca MKⅡ基因表达水平的变化。结果与空白组比较,脾气虚7 d、14 d、21 d组大鼠一般生存状况较差,脾虚宏观证候积分显著升高(P<0.05),平均每日摄食量、平均每日体重增加量和负重游泳耐力降低(P<0.05),骨骼肌组织Ca M、Ca MKⅡ基因相对表达量显著降低,且以脾气虚模型21 d组变化显著(P<0.05)。结论脾气虚大鼠骨骼肌组织Ca M信号通路中Ca M、Ca MKⅡ基因表现为低表达水平。
Objective To investigate the expression of CaM and CaM Ⅱ in calmodulin signaling pathway of spleen deficiency rats. Methods The experimental animals were randomly divided into blank group and spleen deficiency model group (7 d, 14 d and 21 d groups) with 10 in each group. In addition to the blank group, the remaining animals were used to establish the rat model of spleen-qi deficiency syndrome by complex method (bitter cold and dampness method, exhaustion method and dystrophy). After observing the general survival state of rats in each group, Time points, average daily intake, average body weight gain, and endurance swimming load at the same time, real-time fluorescent quantitative PCR was used to detect the changes of Ca M, Ca MKⅡ gene expression in skeletal muscle Ca M signaling pathway. Results Compared with the blank group, the general survival status of the rats on the 7th, 14th and 21st day of spleen deficiency were worse than those of the blank group, and the macroscopic syndrome scores were significantly increased (P <0.05), the average daily food intake and the average daily weight gain (P <0.05). The relative expression of CaM and CaMKII gene in skeletal muscle significantly decreased (P <0.05). Conclusions Ca M and Ca MKⅡ genes in CaM signaling pathway in skeletal muscle of spleen deficiency rats showed low expression level.