Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy
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Chunxia Chen1,*, Wan Chen2,*, Yaoxuan Li3, Yanling Dong3, Xiaoming Teng3, Zhihuan Nong4, Xiaorong Pan1, Liwen Lv2, Ying Gao5 and Guangwei Wu6
1Department of Hyperbaric Oxygen, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, P. R. China
2Department of Emergency, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, P. R. China
3Department of Neurology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, P. R. China
4Department of Pharmacology, Guangxi Institute of Chinese Medicine and Pharmaceutical Science, Nanning, Guangxi 530022, P. R. China
5Department of Biology and Tennessee Center for Botanical Medicine Research, Middle Tennessee State University, Murfreesboro, TN 37132, USA
6Department of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, P. R. China
*These authors have contributed equally to this work
Guangwei Wu, email: email@example.com
Keywords: hyperbaric oxygen; inflammation; autophagy; mammalian target of rapamycin
Received: July 14, 2017 Accepted: August 27, 2017 Published: December 04, 2017
Our previous study demonstrated that hyperbaric oxygen (HBO) preconditioning protected against myocardial ischemia reperfusion injury (MIRI) and improved myocardial infarction. However, HBO’s effect on MIRI-induced inflammation and autophagy remains unclear. In this study, we investigate the potential impact and underlying mechanism of HBO preconditioning on an MIRI-induced inflammatory response and autophagy using a ligation of the left anterior descending (LAD) coronary artery rat model. Our results showed that HBO restored myocardial enzyme levels and decreased the apoptosis of cardiomyocytes, which were induced by MIRI. Moreover, HBO significantly suppressed MIRI-induced inflammatory cytokines. This effect was associated with the inhibition of the TLR4-nuclear factor kappa-B (NF-κB) pathway. Interestingly, lower expression levels of microtubule-associated protein 1 light chain 3B (LC3B) and Beclin-1 were observed in the HBO-treatment group. Furthermore, we observed that HBO reduced excessive autophagy by activating the mammalian target of the rapamycin (mTOR) pathway, as evidenced by higher expression levels of threonine protein kinase (Akt) and phosphorylated-mTOR. In conclusion, HBO protected cardiomocytes during MIRI by attenuating inflammation and autophagy. Our results provide a new mechanistic insight into the cardioprotective role of HBO against MIRI.
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