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目的:观察补肾阳方拮抗外源性糖皮质激素HPA轴抑制及分解代谢的效果及机制。方法:将SD大鼠分为对照组,模型组,模型+补肾阳复方低、中、高剂量组。采用皮质酮注射造成肾阳虚模型。采用ELISA法检测血浆促肾上腺皮质激素(ACTH)、皮质酮浓度;取肾上腺,进行全基因组表达谱芯片检测及分析。结果:糖皮质激素造模导致大鼠体重降低,补肾阳方在第7、14天均能保护体重。补肾阳方治疗使造模组下降的肾上腺重量、ACTH、皮质酮水平升高。基因芯片结果筛选出了模型组上调或下调且能被补肾阳复方逆转的基因828个,功能分析显示涉及类固醇合成酶和细胞增殖通路。结论:补肾阳方保护糖皮质激素肾阳虚证模型的HPA轴功能,并能拮抗糖皮质激素分解效应,保护动物体重。
Objective: To observe the effect and mechanism of Bushenyangfang on antagonizing exogenous glucocorticoid HPA axis inhibition and catabolism. Methods: SD rats were divided into control group, model group, model + Bushenyang compound low, medium and high dose group. Corticosterone injection caused by kidney yang deficiency model. Plasma adrenocorticotropic hormone (ACTH) and corticosterone levels were measured by ELISA. Adrenal gland was taken for whole-genome cDNA microarray detection and analysis. Results: Glucocorticoid induced weight loss in rats. Bushenyang prescription can protect the body weight on the 7th and 14th days. Bushenyangfang makes the adrenal gland weight, ACTH and corticosterone which are decreased by the model making group. Gene chip results screened the model group up or down and can be reversed by the Kidney Yang complex reversal gene 828, functional analysis showed that steroidogenic enzymes and cell proliferation pathway. Conclusion: Bushenyangfang protects the HPA axis of glucocorticoid-induced kidney-Yang deficiency syndrome model and antagonizes the effect of glucocorticoid decomposition and protects the body weight of animals.