Tian Rong, Gong Zi-han, Yang Xiao-yi, Zhu Li-ming, Duan Yong-qiang, Cheng Ying-xia, Du Juan, Wang Yan
Zhongguo Zhong Yao Za Zhi. 2015 Oct;40(20):4075-9.
To observe the dynamic time-phase expressions of key genes of brain-gut CaM signal pathway of spleen Qi deficiency rats and the intervention effect of Sijunzi decoction.
Male Wistar rats were randomly divided into the normal control group, model 14 d, 21 d, 28 d groups, and Sijunzi decoction 14 d, 21 d, 28 d groups. Except for the normal control group, the remaining groups were included into the spleen Qi deficiency model with the bitter cold breaking Qi method (ig 7.5 g · kg⁻¹ · d⁻¹ of Rheum officinale, Fructus aurantii immaturus, Magnolia officinalis preparation) and the exhaustive swimming method. On the 7th day after the modeling, the Sijunzi decoction groups were orally administered with Sijunzi decoction 20 g · kg⁻¹ · d⁻¹. The expressions of key genes CaM/CaMK II of CaM signaling pathway in hippocampus and intestine at different time points by immunohistochemical method and Western blot. At the same time, the intervention effect of Sijunzi decoction on spleen Qi deficiency rats and its mechanism were analyzed.
Spleen Qi deficiency rats showed higher intestinal CaM/CaMK II expression and lower hippocampus CaM/CaMK II expression than normal rats (P < 0.05, P < 0.01). After the treatment of Sijunzi decoction, spleen Qi deficiency rats showed reduction in intestinal CaM/CaMK II expression and increase in hippocampus CaM/CaMK II expression (P < 0.05, P < 0.01).
The formation of spleen Qi deficiency syndrome may be related to the high expression of CaM/CaMK II in small intestine tissues and its low expression in hippocampus tissues. Sijunzi decoction may achieve the therapeutic effect in spleen Qi deficiency syndrome by reducing the CaM/CaMK II expression in intestinal tissues and increasing it in hippocampus tissues.
观察脾气虚证大鼠脑肠CaM信号通路关键基因的动态时相表达及四君子汤的干预作用。
将雄性Wistar大鼠随机分为正常对照组、模型14 d组、模型21 d组、模型28 d组、四君子汤14 d组、四君子汤21 d组、四君子汤28 d组。除正常对照组外,其余各组采用苦寒泻下法(ig大黄、枳实、厚朴制剂7.5 g·kg⁻¹·d⁻¹)结合力竭游泳法制备脾气虚证模型。造模后第7天,四君子汤组大鼠灌胃给予四君子汤20 g·kg⁻¹·d⁻¹。采用免疫组化法和Western blot法检测不同时间点海马和肠道中CaM信号通路关键基因CaM/CaMK II的表达。同时,分析四君子汤对脾气虚证大鼠的干预作用及其机制。
脾气虚证大鼠肠道CaM/CaMK II表达高于正常大鼠,海马CaM/CaMK II表达低于正常大鼠(P<0.05,P<0.01)。四君子汤治疗后,脾气虚证大鼠肠道CaM/CaMK II表达降低,海马CaM/CaMK II表达升高(P<0.05,P<0.01)。
脾气虚证的形成可能与小肠组织中CaM/CaMK II高表达及海马组织中低表达有关。四君子汤可能通过降低肠道组织中CaM/CaMK II表达、升高海马组织中CaM/CaMK II表达而发挥对脾气虚证的治疗作用。