caa a22 4500 606236317 CHVBK 20210128101247.0 cr unu---uuuuu 210128e20150801xx s 000 0 eng 10.1007/s11010-015-2439-6 doi (NATIONALLICENCE)springer-10.1007/s11010-015-2439-6 Contribution of mitochondrial function to exercise-induced attenuation of renal dysfunction in spontaneously hypertensive rats [Elektronische Daten] [Qi Gu, Li Zhao, Yan-Ping Ma, Jian-Dong Liu] It is well known that exercise training exhibits renal protective effects in animal models of hypertension and chronic renal failure. However, the mechanisms regulating these effects of exercise training remain unclear. This study aimed to investigate the role of mitochondrial function in exercise-induced attenuation of renal injury in spontaneously hypertensive rats (SHR). The adult male SHR and age-matched normotensive Wistar-Kyoto rats (WKY) were given moderate-intensity exercise for 12weeks or treated with MitoQ10 for 8weeks. In this work, exercise training in SHR reduced blood pressure, and effectively attenuated renal dysfunction, marked by reduced creatinine excretion, albuminuria, blood urea nitrogen, and glomerular sclerosis. Exercise training in SHR reduced MDA levels in plasma and kidneys and suppressed formation of 3-nitrotyrosine in kidneys. Exercise training suppressed mitochondrial ROS and $${\text{O}}_2^ - $$ O 2 - formation, enhanced ATP formation, reduced mitochondrial swelling, and restored electron transport chain enzyme activity in kidneys of SHR. Furthermore, exercise training upregulated protein expression of uncoupling protein 2 and manganese superoxide dismutase in kidneys of SHR. In addition, treatment with mitochondria-targeted antioxidant MitoQ10 exhibited similar renal protective effects in SHR. In conclusion, chronic aerobic exercise training preserved mitochondrial function and abated oxidative stress in the kidneys of SHR, which may in part explain the protective effect of exercise on renal function and structure in hypertensive individuals. Springer Science+Business Media New York, 2015 Hypertension nationallicence Oxidative stress nationallicence Mitochondria nationallicence Kidney nationallicence Exercise nationallicence Gu Qi School of Physical Education, Xi'an Technological University, 4 Jinhua Road, 710032, Xi'an, Shaanxi Province, China aut Zhao Li School of Physical Education, LuoyangNormalUniversity, Luoyang, Henan Province, China aut Ma Yan-Ping Department of Neurology, Chengyang People's Hospital, Qingdao, Shandong Province, China aut Liu Jian-Dong Department of Gastroenterology, The Third People's Hospital of Datong, Datong, Shanxi Province, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 406/1-2(2015-08-01), 217-225 0300-8177 406:1-2<217 2015 406 11010 https://doi.org/10.1007/s11010-015-2439-6 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-015-2439-6 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Gu Qi School of Physical Education, Xi'an Technological University, 4 Jinhua Road, 710032, Xi'an, Shaanxi Province, China aut NATIONALLICENCE 700 1- Zhao Li School of Physical Education, LuoyangNormalUniversity, Luoyang, Henan Province, China aut NATIONALLICENCE 700 1- Ma Yan-Ping Department of Neurology, Chengyang People's Hospital, Qingdao, Shandong Province, China aut NATIONALLICENCE 700 1- Liu Jian-Dong Department of Gastroenterology, The Third People's Hospital of Datong, Datong, Shanxi Province, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 406/1-2(2015-08-01), 217-225 0300-8177 406:1-2<217 2015 406 11010