【摘要】 目的:研究NADPH氧化酶抑制剂apocynin对力竭运动大鼠运动性蛋白尿产生的影响及其机制。方法:32只SD雄性大鼠随机分为安静对照组(C组)、对照+药物组(CA组)、力竭运动组(E组)、力竭运动+药物组(EA组)。药物注射按10 mg/kg体重,每天一次,连续3 d,并在末次药物注射1 h后进行一次性跑台力竭运动。测定运动后尿UP、血液BUN水平、肾脏ROS浓度、NOS活性、NOS与3-NT蛋白含量。结果:结果显示,E组UP、肾脏ROS、iNOS含量及活性、3-NT明显升高,而EA组的这些指标与C组相比无显著性差异。结论:力竭运动可明显增加肾组织NADPH氧化酶活性,从而产生大量的ROS,后者可迅速地与由肾脏iNOS催化生成的NO反应,产生过量的ONOO-,诱发运动性蛋白尿的生成。更多还原

【Abstract】 Objective:To investigate the effect of NADPH oxidase inhibitor apocynin on exercise-induced proteinuria and its related mechanism. Methods:Thirty-two SD rats were randomly divided into the control group(group C),control + drug group(group CA),exhaustive exercise group(group E),exhaustive exercise + drug group(group EA). The rats were administrated apocynin at 10 mg / kg weight,once a day for three days,and one hour after the drug injection,a one-time exhaustive exercise was performed. After exhaustive exercise,urine protein,blood urea nitrogen(BUN),and kidney reactive oxygen species(ROS)concentration,NOS activity,NOS and 3-NT concentration were detected. Results:In comparison to control group urinary protein(UP),ROS,inductible nitric oxide synthase(iNOS),3-NT levels increased significantly in group E while those in group EA did not change. Conclusion:The elevated renal NADPH oxidase activity by exhaustive exercise induced ROS that can rapidly react with NO,and then produces excess peroxynitrite,which contributes to occurrence of exercise-induced proteinuria.更多还原