Hydrogen Gas Attenuates Myocardial Ischemia Reperfusion Injury Independent of Postconditioning in Rats by Attenuating Endoplasmic Reticulum Stress-Induced Autophagy

Background/Aims: To study the effect of inhaling hydrogen gas on myocardial ischemic/reperfusion(I/R) injury in rats. Methods: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plu...

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Veröffentlicht in:Cellular physiology and biochemistry 2017-01, Vol.43 (4), p.1503-1514
Hauptverfasser: Gao, Yunan, Yang, Hongxiao, Chi, Jing, Xu, Qiannan, Zhao, Luqi, Yang, Weijia, Liu, Weifan, Yang, Wei
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container_start_page 1503
container_title Cellular physiology and biochemistry
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creator Gao, Yunan
Yang, Hongxiao
Chi, Jing
Xu, Qiannan
Zhao, Luqi
Yang, Weijia
Liu, Weifan
Yang, Wei
description Background/Aims: To study the effect of inhaling hydrogen gas on myocardial ischemic/reperfusion(I/R) injury in rats. Methods: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH 2 ) and the ischemic postconditioning plus hydrogen group (IPoH 2 ). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour. Followed by 2 hours of reperfusion. In the IPo and IPoH2 group, four cycles of 1 min reperfusion/1 min ischemia was given at the end of 1 hour coronary occlusion. While 2% hydrogen was administered by inhalation 5 min before reperfusion till 2 hours after reperfusion in both the IPoH2 and IH2 group. The heart and blood samples were harvested at the end of the surgical protocol. Then the myocardium cell endoplasmic reticulum(ER) stress and autophagy was observed by electron microscope. In addition, the cardiac ER stress and autophagy related proteins expression were detected by Western blotting analysis. Results: Both inhaling 2% hydrogen and ischemic postconditioning treatment reduced the ischemic size and serum troponin I level in rats with I/R injury, and inhaling hydrogen showed a more curative effect compared with ischemic postconditioning treatment. Meanwhile inhaling hydrogen showed a better protective effect in attenuating tissue reactive oxygen species. Malondialdehyde levels and immunoreactivities against 8-hydroxy-2’-deoxyguanosine and inhibiting cardiac endoplasmic reticulum stress and down-regulating autophagy as compared with ischemic postconditioning treatment. Conclusion: These results revealed a better protective effect of hydrogen on myocardial ischemic/reperfusion injury in rats by attenuating endoplasmic reticulum stress and down-regulating autophagy compared with ischemic postconditioning treatment.
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Methods: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH 2 ) and the ischemic postconditioning plus hydrogen group (IPoH 2 ). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour. Followed by 2 hours of reperfusion. In the IPo and IPoH2 group, four cycles of 1 min reperfusion/1 min ischemia was given at the end of 1 hour coronary occlusion. While 2% hydrogen was administered by inhalation 5 min before reperfusion till 2 hours after reperfusion in both the IPoH2 and IH2 group. The heart and blood samples were harvested at the end of the surgical protocol. Then the myocardium cell endoplasmic reticulum(ER) stress and autophagy was observed by electron microscope. In addition, the cardiac ER stress and autophagy related proteins expression were detected by Western blotting analysis. Results: Both inhaling 2% hydrogen and ischemic postconditioning treatment reduced the ischemic size and serum troponin I level in rats with I/R injury, and inhaling hydrogen showed a more curative effect compared with ischemic postconditioning treatment. Meanwhile inhaling hydrogen showed a better protective effect in attenuating tissue reactive oxygen species. Malondialdehyde levels and immunoreactivities against 8-hydroxy-2’-deoxyguanosine and inhibiting cardiac endoplasmic reticulum stress and down-regulating autophagy as compared with ischemic postconditioning treatment. Conclusion: These results revealed a better protective effect of hydrogen on myocardial ischemic/reperfusion injury in rats by attenuating endoplasmic reticulum stress and down-regulating autophagy compared with ischemic postconditioning treatment.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000481974</identifier><identifier>PMID: 29035876</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Apoptosis ; Autophagy ; Autophagy - drug effects ; Cytotoxicity ; Endoplasmic reticulum ; Endoplasmic reticulum stress ; Endoplasmic Reticulum Stress - drug effects ; Heart attacks ; Hospitals ; Hydrogen ; Hydrogen - therapeutic use ; Ischemia ; Ischemic Postconditioning ; Ischemic/reperfusion injury ; Kinases ; Laboratory animals ; Male ; Metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - therapy ; Myocardium - pathology ; Original Paper ; Oxidative stress ; Proteins ; Rats, Wistar ; Rodents ; Ventilation</subject><ispartof>Cellular physiology and biochemistry, 2017-01, Vol.43 (4), p.1503-1514</ispartof><rights>2017 The Author(s). Published by S. Karger AG, Basel</rights><rights>2017 The Author(s). Published by S. 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Methods: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH 2 ) and the ischemic postconditioning plus hydrogen group (IPoH 2 ). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour. Followed by 2 hours of reperfusion. In the IPo and IPoH2 group, four cycles of 1 min reperfusion/1 min ischemia was given at the end of 1 hour coronary occlusion. While 2% hydrogen was administered by inhalation 5 min before reperfusion till 2 hours after reperfusion in both the IPoH2 and IH2 group. The heart and blood samples were harvested at the end of the surgical protocol. Then the myocardium cell endoplasmic reticulum(ER) stress and autophagy was observed by electron microscope. 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Methods: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH 2 ) and the ischemic postconditioning plus hydrogen group (IPoH 2 ). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour. Followed by 2 hours of reperfusion. In the IPo and IPoH2 group, four cycles of 1 min reperfusion/1 min ischemia was given at the end of 1 hour coronary occlusion. While 2% hydrogen was administered by inhalation 5 min before reperfusion till 2 hours after reperfusion in both the IPoH2 and IH2 group. The heart and blood samples were harvested at the end of the surgical protocol. Then the myocardium cell endoplasmic reticulum(ER) stress and autophagy was observed by electron microscope. In addition, the cardiac ER stress and autophagy related proteins expression were detected by Western blotting analysis. Results: Both inhaling 2% hydrogen and ischemic postconditioning treatment reduced the ischemic size and serum troponin I level in rats with I/R injury, and inhaling hydrogen showed a more curative effect compared with ischemic postconditioning treatment. Meanwhile inhaling hydrogen showed a better protective effect in attenuating tissue reactive oxygen species. Malondialdehyde levels and immunoreactivities against 8-hydroxy-2’-deoxyguanosine and inhibiting cardiac endoplasmic reticulum stress and down-regulating autophagy as compared with ischemic postconditioning treatment. Conclusion: These results revealed a better protective effect of hydrogen on myocardial ischemic/reperfusion injury in rats by attenuating endoplasmic reticulum stress and down-regulating autophagy compared with ischemic postconditioning treatment.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29035876</pmid><doi>10.1159/000481974</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Apoptosis
Autophagy
Autophagy - drug effects
Cytotoxicity
Endoplasmic reticulum
Endoplasmic reticulum stress
Endoplasmic Reticulum Stress - drug effects
Heart attacks
Hospitals
Hydrogen
Hydrogen - therapeutic use
Ischemia
Ischemic Postconditioning
Ischemic/reperfusion injury
Kinases
Laboratory animals
Male
Metabolism
Myocardial Reperfusion Injury - pathology
Myocardial Reperfusion Injury - therapy
Myocardium - pathology
Original Paper
Oxidative stress
Proteins
Rats, Wistar
Rodents
Ventilation
title Hydrogen Gas Attenuates Myocardial Ischemia Reperfusion Injury Independent of Postconditioning in Rats by Attenuating Endoplasmic Reticulum Stress-Induced Autophagy
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