摘要
目的研究腺嘌呤对大鼠肾脏AT1R、MR mRNA及蛋白表达的影响,探讨其导致"肾虚多尿"的分子药理学机制。方法利用酶联免疫分析法分别检测正常组、腺嘌呤组动物血中血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)的含量;RT-PCR与免疫组化的方法检测各组动物肾脏AT1R、MR mRNA及蛋白的表达。结果与正常组比较,腺嘌呤可减少大鼠血中AngⅡ、ALD(0.119±0.026、193.94±65.09),差异有非常显著意义(P<0.01);可明显下调大鼠肾脏AT1R、MR mRNA及蛋白的表达(P<0.01)。结论腺嘌呤所致"肾虚多尿"的发生可能与肾脏AT1R、MR基因表达的下调和AT1R、MR蛋白表达的减少,ALD合成与分泌减少或功能下降,继而调节水液代谢的作用减弱密切相关。
Objective To study the effect of adenine on renal AT1R and MR mRNA and protein expression in rats, and to explore the molecular pharmacological mechanism of adenine in inducing kidney deficiency. Methods Enzyme-linked immunosorbent assay was used to detect the blood levels of angiotensin Ⅱ fAng Ⅱ）and aldosterone（ALD） in the normal group and adenine group. RT-PCR and immunohistochemistry were used to examine mRNA and protein expression of renal AT1R and MR in rats. Results Compared with the normal group, adenine could remarkedly decrease the blood contents of Ang Ⅱ and ALD in rats, and down-regulated renal mRNA and protein expression of AT1R and MR （P 〈 0.01 ）. Conclusion Adenine can down-regulate the mRNA and protein expression of AT1R and MR in rats, decrease the blood content of ALD, and regulate the water metabolism, which contributes to the patho- genesis of adenine-induced kidney-deficiency hyperdiuresis.
出处
《中药新药与临床药理》
CAS
CSCD
北大核心
2010年第4期337-340,共4页
Traditional Chinese Drug Research and Clinical Pharmacology
基金
国家自然科学基金项目(30873425)
