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目的:研究别嘌呤醇对附子在腺嘌呤所致慢性肾衰模型和一氧化氮合酶(NOS)抑制型高血压模型中的影响,并初步探讨其作用机制。方法:将雄性清洁级小鼠随机分为对照组、模型组、别嘌呤醇组(A)和别嘌呤醇附子组(FA)。对照组小鼠灌胃给予蒸馏水,其余各组小鼠持续4周隔天灌胃给予腺嘌呤,从第3周开始灌胃给予相应药物即别嘌呤醇(70mg/kg)、附子水煎剂(腺嘌呤模型为5g/kg,L-NNA模型为3g/kg)。记录小鼠一般情况,第4周末测定小鼠血清一氧化氮(NO),心组织蛋白、一氧化氮(NO)、丙二醛(MDA),肝肾组织蛋白、一氧化氮(NO)、丙二醛(MDA)、尿酸(UA)含量。结果:与对照组相比,腺嘌呤模型组小鼠体重下降,摄食量减少,饮水量升高。与模型组相比,A组和FA组小鼠生化指标具有一定的改善,肾系数、小鼠血清、心、肝和肾组织NO和肝、肾组织UA、肝组织MDA降低了,肾组织MDA升高,其中FA组小鼠NO含量显著高于A组。L-NNA模型中,与对照组相比,模型组小鼠体重下降,摄食量和饮水量减少。与A组相比,FA组血清、心、肝和肾组织NO,肝和肾组织UA升高。在两种模型中,肝和肾组织中NO上升的幅度显著大于UA的上升幅度。综合结果表明腺嘌呤模型中FA组小鼠表现出显著的肾功能改善作用,L-NNA模型中FA组小鼠表现出肾功能损伤加重作用。结论:附子可能是通过激活肾素血管紧张素系统升高两种模型中血清、肝肾组织的NO含量。
Objective: To investigate the effects of allopurinol on the model of chronic renal failure induced by adenine and nitric oxide synthase (NOS) in hypertensive rats model induced by adenine, and to explore its mechanism. Methods: Male mice were randomly divided into control group, model group, allopurinol group (A) and allopurinol group (FA). The mice in the control group were given gavage with distilled water. The remaining mice in each group were given adenine orally by gavage every other day for 4 weeks. The corresponding drugs, ie allopurinol (70mg / kg) Adenine model 5g / kg, L-NNA model 3g / kg). At the end of the 4th week, the levels of serum NO, cardiac tissue protein, NO, MDA, liver and kidney tissue protein, nitric oxide (NO), malondialdehyde Malondialdehyde (MDA), uric acid (UA) content. Results: Compared with the control group, adenine model mice decreased body weight, food intake decreased, drinking water increased. Compared with the model group, the biochemical indexes of the mice in group A and group FA improved to a certain degree. The renal coefficient, the serum NO, liver and kidney, UA in liver and kidney, The NO content in FA group was significantly higher than that in A group. L-NNA model, compared with the control group, model mice decreased body weight, food intake and decreased drinking water. Compared with group A, NO, liver and kidney UA in serum, heart, liver and kidney of FA group increased. In both models, the magnitude of NO increase in liver and kidney tissue was significantly greater than the rise in UA. The comprehensive results showed that FA group mice showed significant renal function improvement in adenine model, and FA group mice showed aggravating renal function injury in L-NNA model. Conclusion: Aconite may increase serum NO, liver and kidney NO levels in both models by activating renin-angiotensin system.