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。
Objective: To investigate the effect of NADPFI 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, induc, tible 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 oeemTence of exerciseinduced proteinuria.
出处
《中国应用生理学杂志》
CAS
CSCD
2016年第2期116-120,共5页
Chinese Journal of Applied Physiology
基金
湖南省自然科学基金资助(12JJ3093)
关键词
NADPH氧化酶
运动性蛋白尿
活性氧
过氧亚硝基阴离子
一氧化氮
NADPH oxidase
exercise-induced proteinuria
reactive oxygen species (ROS)
peroxynitrite (ONOO-)
nitric oxide