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Remote Limb Ischaemic Postconditioning Protects Against Myocardial Ischaemia/Reperfusion Injury in Mice: Activation of JAK/STAT3-Mediated Nrf2-Antioxidant Signalling
| Content Provider | Semantic Scholar |
|---|---|
| Author | Gao, Sumin Zhan, Leyun Yang, Zhengchao Shi, Ruili Li, Haobo Xia, Zhengyuan Yuan, Shi-Ying Wu, Qing-Ping Wang, Tingting Yao, Shanglong |
| Copyright Year | 2017 |
| 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. |
| Starting Page | 1140 |
| Ending Page | 1151 |
| Page Count | 12 |
| File Format | PDF HTM / HTML |
| DOI | 10.1159/000481755 |
| Alternate Webpage(s) | http://hub.hku.hk/bitstream/10722/250246/1/content.pdf |
| PubMed reference number | 28977786 |
| Alternate Webpage(s) | https://doi.org/10.1159/000481755 |
| Journal | Medline |
| Volume Number | 43 |
| Journal | Cellular Physiology and Biochemistry |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
