脾阳虚大鼠下丘脑和小肠缩胆囊素信号转导途径的变化研究

Changes of Cholecycstokinin Transmembrane Signal Pathway in Hypothalamus and Small Intestine in Spleen Yang Deficiency

目的：通过检测下丘脑和小肠组织缩胆囊素（Cholecystokinin,CCK）信号转导途径的变化,研究脾阳虚的发生机制。方法：16只SD大鼠随机分为对照组和脾阳虚组（模型组）,每组8只; ELISA法检测下丘脑和小肠组织CCK-8、环-磷酸腺苷（cycle monophosphate,c AMP）和蛋白激酶A（protein kinase A,PKA）含量;免疫组化法检测下丘脑CCK2受体（CCK 2 receptor,CCK2R）和小肠CCK1R表达。结果：与对照组相比,下丘脑和小肠CCK-8水平明显升高,而下丘脑的CCKR2表达、c AMP和PKA水平以及小肠CCKR1表达和c AMP水平均显著下降,但小肠PKA水平没有明显变化。结论：脾阳虚的发生与下丘脑和小肠组织中CCK过度释放有关。

Objective： To explore the mechanism of spleen Yang deficiency focusing on cholecycstokinin（CCK） transmembrane signal pathway. Methods： Sixteen SD rats were randomly divided into the control and spleen Yang deficiency groups,8 rats in each group. ELISA was used to check CCK-8,c AMP and PKA concentrations in hypothalamic and small intestine（SI）. The immunohistochemistry was used to detect CCK 2 receptor（CCK2 R） in hypothalamic tissue and CCK1 R in SI tissues. Results： Compared with those in the control group,CCK-8 levels in hypothalamic and SI tissues were increased. The hypothalamic CCK2 R expression and levels of c AMP and PKA,and SI CCK1 R expression and c AMP level were all reduced,but there was no overt change in SI PKA level in the model group. Conclusion： Overrelease of CCK in hypothalamus and SI tissues might be contribute to the development of spleen Yang deficiency.