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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 the expression of AT1R, MR mRNA and protein in rat kidney and to explore the molecular pharmacological mechanism of adenine induced renal hyperuria. Methods The contents of angiotensin Ⅱ (Ang Ⅱ) and aldosterone (ALD) in the blood of normal and adenine groups were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of AT1R, mRNA and protein expression. Results Compared with the normal group, adenine decreased Ang Ⅱ, ALD (0.119 ± 0.026, 193.94 ± 65.09) in the blood of the rats, and the difference was significant (P <0.01); adenine could significantly reduce the expression of AT1R, MR mRNA and protein (P <0.01). Conclusions Adenine-induced “kidney-polyuria” may be related to the down-regulation of AT1R and MR mRNA expression, the decrease of AT1R and MR protein expressions, the reduction or loss of ALD synthesis and secretion, and the decrease of water-liquid metabolism closely related.