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Article: Remote Limb Ischaemic Postconditioning Protects Against Myocardial Ischaemia/Reperfusion Injury in Mice: Activation of JAK/STAT3-Mediated Nrf2-Antioxidant Signalling
Title | Remote Limb Ischaemic Postconditioning Protects Against Myocardial Ischaemia/Reperfusion Injury in Mice: Activation of JAK/STAT3-Mediated Nrf2-Antioxidant Signalling |
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Authors | |
Keywords | Akt ENOS HO-1 JAK/STAT3 Nrf2 Remote limb ischaemic postconditioning |
Issue Date | 2017 |
Publisher | Karger Publishers Open Access. The Journal's web site is located at http://www.karger.com/CPB |
Citation | Cellular Physiology and Biochemistry, 2017, v. 43 n. 3, p. 1140-1151 How to Cite? |
Abstract | BACKGROUND: This study aimed to evaluate the protective effect and mechanisms of remote limb ischaemic postconditioning (RIPostC) against myocardial ischaemia/reperfusion (IR) injury. METHODS: Male mice underwent 45 min of coronary artery occlusion followed by 2 h of reperfusion. RIPostC was achieved by three cycles of 5 min of ischaemia and 5 min of reperfusion in the left hind limb at the start of the reperfusion period. After 2 h of cardiac reperfusion, myocardial infarct size, cardiac enzyme release, apoptosis and oxidative stress were assessed. Protein expression and phosphorylation were measured by Western blotting. RESULTS: RIPostC significantly decreased cardiac IR injury, as reflected by reduced infarct size and cellular apoptosis (22.9 ± 3.3% vs 40.9 ± 6.2% and 13.4% ± 3.1% vs 26.2% ± 3.1%, respectively, both P < 0.01) as well as plasma creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) release (21.97 ± 4.08 vs 35.86 ± 2.91 ng/ml and 6.17 ± 0.58 vs 8.37 ± 0.89 U/ml, respectively, both P < 0.01) compared with the IR group. RIPostC significantly increased the phosphorylation of myocardial STAT3, Akt and eNOS (P < 0.01). In addition, RIPostC elevated the nuclear translocation of Nrf2 and the expression of HO-1 and reduced myocardial oxidative stress (P < 0.05). Interestingly, pretreatment with the JAK/STAT3 inhibitor AG490 blocked the cardioprotective effect of RIPostC accompanied by decreased phosphorylation of myocardial STAT3, Akt and eNOS (P < 0.05), decreased nuclear translocation of Nrf2 and expression of HO-1, as well as increased oxidative stress (P < 0.05). CONCLUSION: RIPostC attenuates apoptosis and protects against myocardial IR injury, possibly through the activation of JAK/STAT3-mediated Nrf2-antioxidant signalling. |
Persistent Identifier | http://hdl.handle.net/10722/250246 |
ISSN | 2023 Impact Factor: 2.5 2023 SCImago Journal Rankings: 0.733 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Gao, S | - |
dc.contributor.author | Zhan, L | - |
dc.contributor.author | Yang, Z | - |
dc.contributor.author | Shi, R | - |
dc.contributor.author | Li, H | - |
dc.contributor.author | Xia, Z | - |
dc.contributor.author | Yuan, S | - |
dc.contributor.author | Wu, QP | - |
dc.contributor.author | Wang, T | - |
dc.contributor.author | Yao, S | - |
dc.date.accessioned | 2017-12-20T09:22:56Z | - |
dc.date.available | 2017-12-20T09:22:56Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Cellular Physiology and Biochemistry, 2017, v. 43 n. 3, p. 1140-1151 | - |
dc.identifier.issn | 1015-8987 | - |
dc.identifier.uri | http://hdl.handle.net/10722/250246 | - |
dc.description.abstract | BACKGROUND: This study aimed to evaluate the protective effect and mechanisms of remote limb ischaemic postconditioning (RIPostC) against myocardial ischaemia/reperfusion (IR) injury. METHODS: Male mice underwent 45 min of coronary artery occlusion followed by 2 h of reperfusion. RIPostC was achieved by three cycles of 5 min of ischaemia and 5 min of reperfusion in the left hind limb at the start of the reperfusion period. After 2 h of cardiac reperfusion, myocardial infarct size, cardiac enzyme release, apoptosis and oxidative stress were assessed. Protein expression and phosphorylation were measured by Western blotting. RESULTS: RIPostC significantly decreased cardiac IR injury, as reflected by reduced infarct size and cellular apoptosis (22.9 ± 3.3% vs 40.9 ± 6.2% and 13.4% ± 3.1% vs 26.2% ± 3.1%, respectively, both P < 0.01) as well as plasma creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) release (21.97 ± 4.08 vs 35.86 ± 2.91 ng/ml and 6.17 ± 0.58 vs 8.37 ± 0.89 U/ml, respectively, both P < 0.01) compared with the IR group. RIPostC significantly increased the phosphorylation of myocardial STAT3, Akt and eNOS (P < 0.01). In addition, RIPostC elevated the nuclear translocation of Nrf2 and the expression of HO-1 and reduced myocardial oxidative stress (P < 0.05). Interestingly, pretreatment with the JAK/STAT3 inhibitor AG490 blocked the cardioprotective effect of RIPostC accompanied by decreased phosphorylation of myocardial STAT3, Akt and eNOS (P < 0.05), decreased nuclear translocation of Nrf2 and expression of HO-1, as well as increased oxidative stress (P < 0.05). CONCLUSION: RIPostC attenuates apoptosis and protects against myocardial IR injury, possibly through the activation of JAK/STAT3-mediated Nrf2-antioxidant signalling. | - |
dc.language | eng | - |
dc.publisher | Karger Publishers Open Access. The Journal's web site is located at http://www.karger.com/CPB | - |
dc.relation.ispartof | Cellular Physiology and Biochemistry | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Akt | - |
dc.subject | ENOS | - |
dc.subject | HO-1 | - |
dc.subject | JAK/STAT3 | - |
dc.subject | Nrf2 | - |
dc.subject | Remote limb ischaemic postconditioning | - |
dc.title | Remote Limb Ischaemic Postconditioning Protects Against Myocardial Ischaemia/Reperfusion Injury in Mice: Activation of JAK/STAT3-Mediated Nrf2-Antioxidant Signalling | - |
dc.type | Article | - |
dc.identifier.email | Xia, Z: zyxia@hkucc.hku.hk | - |
dc.identifier.authority | Xia, Z=rp00532 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1159/000481755 | - |
dc.identifier.scopus | eid_2-s2.0-85030659043 | - |
dc.identifier.hkuros | 283654 | - |
dc.identifier.volume | 43 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 1140 | - |
dc.identifier.epage | 1151 | - |
dc.identifier.isi | WOS:000416221300022 | - |
dc.publisher.place | Switzerland | - |
dc.identifier.issnl | 1015-8987 | - |