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Wang Y, Liu MZ, Li HJ, et al. [Effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats and the role of Erk1/2 signaling pathway]. Nan Fang Yi Ke Da Xue Xue Bao. 2017;37(8):1028-1034
Wang, Y., Liu, M. Z., Li, H. J., Zhang, W. P., Gao, Q., & Li, Z. H. (2017). [Effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats and the role of Erk1/2 signaling pathway]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 37(8), 1028-1034.
Wang, Ya, et al. "[Effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats and the role of Erk1/2 signaling pathway]." Nan fang yi ke da xue xue bao = Journal of Southern Medical University vol. 37,8 (2017): 1028-1034.
Wang Y, Liu MZ, Li HJ, Zhang WP, Gao Q, Li ZH. [Effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats and the role of Erk1/2 signaling pathway]. Nan Fang Yi Ke Da Xue Xue Bao. 2017 Aug 20;37(8):1028-1034. Chinese. PMID: 28801281; PMCID: PMC6765742.
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Nan Fang Yi Ke Da Xue Xue Bao. 2017 Aug 20;37(8):1028-1034.

[Effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats and the role of Erk1/2 signaling pathway].

Nan fang yi ke da xue xue bao = Journal of Southern Medical University

[Article in Chinese]
Ya Wang, Ming-Zhu Liu, Hong-Jun Li, Wei-Ping Zhang, Qin Gao, Zheng-Hong Li

Affiliations

  1. Department of Physiology, Bengbu Medical College, Bengbu 233030, China. E-mail: [email protected].

PMID: 28801281 PMCID: PMC6765742

Abstract

OBJECTIVE: To investigate the effect of postischemic treatment with endomorphin-1 (EM-1) against myocardial ischemia/reperfusion (IR) injury in rats and on extracellular signal regulated kinase 1/2 (Erk1/2)-dependent signaling pathway.

METHODS: Sprague-Dawley rats were randomly divided into 5 groups, namely the sham-operated group, IR group, EM-1 post-treatment group (EM50 group), EM-1 post-treatment group with PD98059 treatment (EM50+PD group), and PD98059 post-treatment group (PD group). The hemodynamic indexes of the rats were recorded. After reperfusion, CK-MB, LDH, CTnI, MDA, IL-6, TNF-α, and SOD activities or contents were measured, the infarct size was determined, and the expression levels of Erk1/2, P-Erk1/2 and cleaved caspase-3 were detected using Western blotting.

RESULTS: Compared with the sham group, the IR group showed significantly decreased heart rate and mean arterial pressure (P<0.05), which were increased obviously by EM-1 post-treatment (P<0.05). EM-1 post-treatment also resulted in significantly decreased LDH, CK-MB, CTnI, MDA, IL-6, and TNF-α activities or contents (P<0.05), increased SOD activity (P<0.05), reduced the infarct size (P<0.05), and increased the expression level of P-Erk protein (P<0.05). Compared with EM50 group, EM50+PD group showed significantly decreased heart rate and mean arterial pressure (P<0.05), increased LDH, CK-MB, CTnI, MDA, IL-6, and TNF-α activities or contents (P<0.05), decreased SOD activity, increased infarct size (P<0.05), and lowered expression of P-Erk protein (P<0.05).

CONCLUSION: Postischemic treatment with EM-1 protects the heart against IR injury by improving the cardiac function, inhibiting inflammation, and inhibiting oxidative stress and myocardial apoptosis, and Erk1/2 signaling pathway may be involved in this process.

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