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目的:探讨中药复方安神定志灵对注意缺陷多动障碍动物模型SHR大鼠前额叶、纹状体中Gαs、Gαi及Golf mRNA和蛋白表达的影响。方法:将SHR大鼠运用随机区组分为模型组、利他林组、安神定志灵低剂量、中剂量、高剂量组,每组10只,另将10只WKY大鼠设为正常组。安神定志灵低、中、高剂量组分别按生药量6.7、13.4、26.7 g·kg~(-1)灌胃,每日2次;利他林组以2 mg·kg~(-1)给予利他林灌胃,每日2次;模型组和正常对照组每日按体质量给予等量双蒸水灌胃,灌胃4周后处死。分别用RT-PCR和Western Blot检测各组大鼠前额叶、纹状体中Gαs、Golf及Gαi mRNA和蛋白的表达水平。结果:模型组大鼠除前额叶皮质Gαi蛋白外,余G蛋白亚基mRNA和蛋白表达水平均明显低于正常组(P<0.05或P<0.01)。经治疗后,利他林组和安神定志灵各剂量组有提高前额叶皮质、纹状体中三种G蛋白亚基Gαi mRNA和蛋白的表达水平趋势或能显著提高其表达水平(P<0.05或P<0.01)。结论:安神定志灵可以升高SHR大鼠前额叶皮质、纹状体Gαs、Golf及Gαi三者mRNA和蛋白的表达水平,提示安神定志灵可以激活突触后膜多巴胺受体下游不同的G蛋白亚基,进而影响下游的信号通路从而发挥治疗作用。
Objective: To investigate the effects of Anshen Dingzhi Ling on Gαs, Gαi and Golf mRNA and protein expression in the prefrontal lobe and striatum of an animal model of attention deficit hyperactivity disorder. Methods: SHR rats were randomly divided into model group, Ritalin group, Anshen Dingzhi low dose group, middle dose group and high dose group, with 10 rats in each group and 10 WKY rats as normal group. Anshen Dingzhi Ling low, medium and high dose groups were given crude drugs 6.7,13.4,26.7 g · kg ~ (-1) gavage, 2 times a day; Ritalin group to 2 mg · kg -1 Ritalin orally, 2 times a day; model group and normal control group according to the body weight to give the same amount of double-distilled water, gavage after 4 weeks and sacrificed. The mRNA and protein expressions of Gαs, Golgi and Gαi in prefrontal and striatum of rats in each group were detected by RT-PCR and Western Blot. Results: Except prefrontal cortex Gαi protein, the mRNA and protein expressions of extracellular G subunit in model group were significantly lower than those in normal group (P <0.05 or P <0.01). After treatment, each dose group of Ritalin and Anshen Dingzhi increased the expression level of Gαi mRNA and protein in prefrontal cortex and striatum, or significantly increased the expression level (P <0.05 Or P <0.01). Conclusion: Anshen Dingzhi can increase the expression of Gαs, Gol and Gαi mRNA and protein in prefrontal cortex, striatum of SHR rats, suggesting that Anshen Dingzhi can activate different postsynaptic dopamine receptors downstream G protein subunits, which in turn affect the downstream signaling pathway to play a therapeutic role.