caa a22 4500 606220925 CHVBK 20210128101126.0 cr unu---uuuuu 210128e20150501xx s 000 0 eng 10.1007/s00380-014-0523-6 doi (NATIONALLICENCE)springer-10.1007/s00380-014-0523-6 Humid heat exposure induced oxidative stress and apoptosis in cardiomyocytes through the angiotensin II signaling pathway [Elektronische Daten] [Xiaowu Wang, Binbin Yuan, Wenpeng Dong, Bo Yang, Yongchao Yang, Xi Lin, Gu Gong] Exposure to humid heat stress leads to the initiation of serious physiological dysfunction that may result in heat-related diseases, including heat stroke, heat cramp, heat exhaustion, and even death. Increasing evidences have shown that the humid heat stress-induced dysfunction of the cardiovascular system was accompanied with severe cardiomyocyte injury; however, the precise mechanism of heat stress-induced injury of cardiomyocyte remains unknown. In the present study, we hypothesized that humid heat stress promoted oxidative stress through the activation of angiotensin II (Ang II) in cardiomyocytes. To test our hypothesis, we established mouse models of humid heat stress. Using the animal models, we found that Ang II levels in serum were significantly up-regulated and that the Ang II receptor AT1 was increased in cardiomyocytes. The antioxidant ability in plasma and heart tissues which was detected by the ferric reducing/antioxidant power assay was also decreased with the increased ROS production under humid heat stress, as was the expression of antioxidant genes (SOD2, HO-1, GPx). Furthermore, we demonstrated that the Ang II receptor antagonist, valsartan, effectively relieved oxidative stress, blocked Ang II signaling pathway and suppressed cardiomyocyte apoptosis induced by humid heat stress. In addition, overexpression of antioxidant genes reversed cardiomyocyte apoptosis induced by Ang II. Overall, these results implied that humid heat stress increased oxidative stress and caused apoptosis of cardiomyocytes through the Ang II signaling pathway. Thus, targeting the Ang II signaling pathway may provide a promising approach for the prevention and treatment of cardiovascular diseases caused by humid heat stress. Springer Japan, 2014 Humid heat stress nationallicence Cardiomyocyte nationallicence Angiotensin II nationallicence Oxidative stress nationallicence Ang II : Angiotensin II nationallicence AOA : Antioxidant ability nationallicence AT1 : Angiotensin receptor 1 nationallicence ELISA : Enzyme linked immunosorbent assay nationallicence FRAP : The ferric reducing/antioxidant power assay nationallicence GPx : Glutathione peroxidase nationallicence HHS : Humid heat stress nationallicence HO-1 : Heme oxygenase 1 nationallicence HRP : Horseradish peroxidase nationallicence JNK : c-Jun amino-terminal kinases nationallicence LDH : Lactate dehydrogenase nationallicence MAPKs : Mitogen-activated protein kinases nationallicence MDA : Malondialdehyde nationallicence NAD(P)H : Nicotinamide-adenine dinucleotide phosphate nationallicence qRT-PCR : Quantitative real-time polymerase chain reaction nationallicence RAS : Renin-angiotensin system nationallicence ROS : Reactive oxygen species nationallicence RT : Room temperature nationallicence SOD : Superoxide dismutase nationallicence TBS : Tris-buffered saline nationallicence TBST : TBS and tween nationallicence TPTZ : Tripyridyl-s-triazine nationallicence Wang Xiaowu Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut Yuan Binbin Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut Dong Wenpeng Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut Yang Bo Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut Yang Yongchao Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut Lin Xi Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut Gong Gu Department of Anesthesiology, General Hospital of Chengdu Military Command, No. 270, Tianhui Road, Jinniu District, 610083, Chengdu, Si Chuang, People's Republic of China aut Heart and Vessels Springer Japan 30/3(2015-05-01), 396-405 0910-8327 30:3<396 2015 30 380 https://doi.org/10.1007/s00380-014-0523-6 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/s00380-014-0523-6 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Wang Xiaowu Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut NATIONALLICENCE 700 1- Yuan Binbin Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut NATIONALLICENCE 700 1- Dong Wenpeng Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut NATIONALLICENCE 700 1- Yang Bo Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut NATIONALLICENCE 700 1- Yang Yongchao Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut NATIONALLICENCE 700 1- Lin Xi Center of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, 510010, Guangzhou, China aut NATIONALLICENCE 700 1- Gong Gu Department of Anesthesiology, General Hospital of Chengdu Military Command, No. 270, Tianhui Road, Jinniu District, 610083, Chengdu, Si Chuang, People's Republic of China aut NATIONALLICENCE 773 0- Heart and Vessels Springer Japan 30/3(2015-05-01), 396-405 0910-8327 30:3<396 2015 30 380