著者

Zhichao Ma Jie Qi Li Gao Jun Zhang

出版者

International Heart Journal Association

雑誌

International Heart Journal (ISSN:13492365)

巻号頁・発行日

vol.61, no.5, pp.1022-1033, 2020-09-29 (Released:2020-09-29)

参考文献数

41

被引用文献数

7

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Cardiac hypertrophy is one of the significant risk factors that result in maladaptive cardiac remodeling and heart failure, and exercise is known to exert cardioprotection. In this research, the cardioprotective function and exercise mechanisms were explored.The rats underwent transverse aortic constriction (TAC) or a sham operation. The rats that received TAC were randomly assigned to five groups: (1) rats subjected to a sham operation as control group (SC), (2) rats that underwent TAC group (TC), (3) TAC and moderate-intensity exercise group (TE), (4) TE plus 3-MA group (TEM), and (5) TE plus Compound C group (TEC). The heart function was measured via echocardiography. Histological analysis and relative protein testing were conducted to analyze collagen deposition and apoptosis. Furthermore, western blot was employed to measure the protein expression of relevant signaling pathways. Impaired cardiac function, interstitial fibrosis, enhanced apoptosis, and ER stress were observed in the TAC-induced left ventricular hypertrophy. Exercise attenuated TAC-induced cardiac dysfunction, interstitial fibrosis, and ER stress-related apoptosis. In addition, exercise significantly improved autophagy and upregulated AMPK phosphorylation. Furthermore, AMPK inhibitor Compound C repressed the activation of AMPK, and autophagy inhibitor 3-methyladenine reversed exercise-induced autophagy. All of these abolished the protection of exercise against cardiac dysfunction and fibrosis induced by TAC.Our results indicated that 4 weeks of treadmill exercise could alleviate pressure overload-induced LV dysfunction and remodeling via an autophagy-dependent mechanism, which was induced by enhancing autophagy through the activation of AMPK.

著者

Yanyan CHENG Jiangdong XUE Chunyu YAO Li GAO Dexing MA Yan LIU Zhigang ZHANG

出版者

公益社団法人 日本獣医学会

雑誌

Journal of Veterinary Medical Science (ISSN:09167250)

巻号頁・発行日

vol.75, no.9, pp.1139-1146, 2013 (Released:2013-10-01)

参考文献数

47

被引用文献数

3 7

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The objective of this study was to evaluate the possible protection of resveratrol against lung injury induced by arsenic trioxide (As2O3). Twenty-four healthy Chinese Dragon Li cats of either sex were randomly divided into four groups: control (1 ml/kg physiological saline), As2O3 (1 mg/kg), resveratrol (3 mg/kg) and resveratrol (3 mg/kg) + As2O3 (1 mg/kg). The resveratrol + As2O3- treated group was given resveratrol 1 hr before As2O3 (1 mg/kg) administration. We found that pretreatment with resveratrol in a clinically comparable dose regimen can reversed the changes in morphological and biochemical parameters induced by As2O3 in the lung. Resveratrol treatment also upregulated the activities of antioxidant enzymes and attenuated As2O3-induced increases in reactive oxygen species, 8-hydroxydeoxyguanosine and malondialdehyde production in the lung. In addition, resveratrol attenuated the As2O3-induced reduction in the ratio of reduced glutathione to oxidized glutathione, the content of total glutathione and lung arsenic burden. These findings indicated that resveratrol can provide significant protection against As2O3-induced oxidative damage.

著者

Yanyan CHENG Jiangdong XUE Chunyu YAO Li Gao Dexing MA Yan LIU Zhigang ZHANG

出版者

公益社団法人 日本獣医学会

雑誌

Journal of Veterinary Medical Science (ISSN:09167250)

巻号頁・発行日

pp.13-0004, (Released:2013-04-16)

被引用文献数

3 7

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The objective of this study was to evaluate the possible protection of resveratrol against lung injury induced by arsenic trioxide (As2O3). Twenty-four healthy Chinese Dragon-Li cats of either sex were randomly divided into four groups: control (1 ml/kg physiological saline), As2O3 (1 mg/kg), resveratrol (3 mg/kg) and resveratrol (3 mg/kg) + As2O3 (1 mg/kg). The resveratrol + As2O3 treated-group was given resveratrol 1 hr before As2O3 (1 mg/kg) administration. We found that pretreatment with resveratrol in a clinically comparable dose regimen can reversed the changes in morphological and biochemical parameters induced by As2O3 in lung. Resveratrol treatment also up-regulated the activities of antioxidant enzymes, and attenuated As2O3-induced increases in reactive oxygen species, 8-hydroxydeoxyguanosine and malondialdehyde production in lung. In addition, resveratrol attenuated the As2O3-induced reduction in the ratio of reduced glutathione to oxidized glutathione, the content of total glutathione and lung arsenic burden. These findings indicated that resveratrol can give a significant protection against As2O3-induced oxidative damage.