期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 158, 期 -, 页码 171-180出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2020.06.038
关键词
Aerobic exercise; Cardiorenal syndrome II; ALCAT1; Oxidative stress; Apoptosis; Irisin; AMPK-Srit1-PGC-1 alpha signaling pathway
资金
- National Natural Science Foundation of China [31671240, 31701039]
- Fundamental Research Funds for the Central Universities [GK201803096]
Aerobic exercise involves in ameliorating kidney injury, but the underlying mechanisms are not fully clarified. In this study, we elucidated the potential mechanisms of aerobic exercise in ameliorating kidney injury following myocardial infarction (MI). In vivo, wildtype and alcat1 knockout mice were used to establish the MI model, and subjected to six-week moderate-intensity aerobic exercise. In vitro, Normal Rat Kidney (NRK) cells treated with H2O2 and recombinant human Irisin (rhIrisin) were used for exploring potential mechanisms. Our results showed that Irisin expression was up-regulated by aerobic exercise in kidneys after MI, while ALCAT1 was reduced. In alcat1 knockout mice, we found that ALCAT1 involved in the progressions of oxidative stress and apoptosis in impaired kidney tissues of MI mice, but aerobic exercise reversed these changes. Furthermore, in vitro, we observed that Irisin inhibited both H2O2-treatment or overexpression of alcat1-induced oxidative stress and apoptosis in NRK cells, partially via AMPK-Sirt1-PGC-1 alpha pathway. These findings reveal that aerobic exercise participates in Yalleviating the levels of oxidative stress and apoptosis in impaired kidney tissues following MI, partially via activating FNDC5/Irisin-AMPK-Sirt1-PGC-1 alpha signaling pathway and inhibiting ALCAT1 expression.
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