以药测证对肾虚和肾阳虚大鼠基因表达谱的比较研究

Comparison of Gene Expression Profiles between Rats of Shen Deficiency Syndrome and Shen-yang Deficiency Syndrome Differentiated According to Therapeutic Efficacy of Drugs Used

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中文关键词: 肾虚肾阳虚下丘脑-垂体-肾上腺-胸腺轴基因表达谱

英文关键词:Shen deficiency Shen-yang deficiency HPAT axis gene expression profile

基金项目:国家自然科学基金项目(No.904090010);上海市科委重点基础研究计划(No.04JC14090);上海市卫生局中医药科研基金(No.2004J014A)

作者	单位
沈自尹	复旦大学附属华山医院中西医结合研究所上海200040
黄建华	复旦大学附属华山医院中西医结合研究所上海200040
陈伟华	复旦大学附属华山医院中西医结合研究所上海200040

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中文摘要:

目的在分子水平揭示肾虚和肾阳虚内涵的异同。方法肾虚证采用自然衰老大鼠模型,肾阳虚证采用皮质酮大鼠模型,均用淫羊藿总黄酮(epi mediumflavonids,EF)以药测证,分别取下丘脑、垂体、肾上腺、淋巴细胞(HPAT)组织,采用Affymetrix公司的大鼠全基因组芯片,各两次重复基因表达谱研究。结果老年大鼠和皮质酮大鼠与青年大鼠比较,在HPAT轴上首先是众多的神经递质显著下调,接下来是生长激素类和性激素类都显著下调,其表达下调的模式呈高度一致,EF能逆转上述基因的表达;但EF在皮质酮大鼠显著上调热休克蛋白(HSP)和细胞色素P450以及促甲状腺激素(TSH)大幅度上调。结论两组大鼠均具有肾虚的内涵,但肾阳的主要物质基础是甲状腺激素促进能量代谢的氧化磷酸化过程。

英文摘要:

ObjectiveTo explore similarity and difference of connotation between Shen deficiency syndrome(SDS)and Shen-yang deficiency syndrome(SYDS)on the molecular level.MethodsThe senescent SD rats and corticosterone-treated rats were adopted for models of SDS and SYDS respectively,their syndrome was differentiated according to the therapeutic efficacy of treatment with epimedium flavonoids(EF).The gene expression profiles of hypothalamas,pituitary,adrenal gland and lymphocytes(HPAT axis)were detected before and after EF treatment using gene chip provided by Affymetrix company.ResultsAs compared with the young rats,the ageing rats and corticosterone-treated rats showed a significant down-regulation in highly consistent pattern,of various neurotransmitters of HPAT axis firstly,followed with that of growth and sex hormone related genes.EF could reverse the above genes expression in both models,and for SYDS model rats,it could also significantly up-regulate the gene expressions of heat shock protein,cytochrome P450 and thyroid stimulating hormone(TSH).ConclusionBoth SDS and SYDS model rats show connotation of Shen deficiency,and the substantial base of Shen-yang deficiency syndrome resides in the process of oxidative phosphorylation of energy metabolism accelerated by thyroid hormone.

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