[Role of Mitochondrial Permeability Transition Pore in Mediating the Effect of Endomorphin-1 Postconditioning Against Myocardial Ischemia-reperfusion Injury in Rats]

Overview

Journal Nan Fang Yi Ke Da Xue Xue Bao

Specialty General Medicine

Date 2018 Jun 13

PMID 29891450

Citations 1

Authors

Yan-Ping Huang

Tian-Hua Yang

Zhi-Yan Jin

Ya Wang

Hong-Wei Ye

Qin Gao

Zheng-Hong Li

Affiliations

Soon will be listed here.

Abstract

Objective: To investigate the role of mitochondrial permeability transition pore (MPTP) opening in mediating the effect of endomorphine-1 postconditioning to alleviate myocardial ischemia-reperfusion (IR) injury in rats.

Methods: Forty-five male SD rats were randomized equally for sham operation, myocardial IR injury, endomorphin-1 postconditioning, atractyloside (a MPTP opener) postconditioning, or endomorphin-1 + atractyloside postconditioning. The hemodynamic param-eters of the rats were monitored in real time via carotid artery cannulation to the left ventricle. After reperfusion, plasma samples were collected for biochemical analyses. The size of myocardial infarct area was detected using Evans blue and TTC double staining, and the myocardial expressions of apoptosis-related proteins Bax, Bcl-2 and cleaved caspase-3 were analyzed using Western blotting.

Results: Myocardial IR injury resulted in significantly decreased heart rate and blood pressure in the rats (P<0.05). Compared with those in IR group, the rats with endomorphin-1 postconditioning showed significantly increased heart rate and blood pressure (P<0.05), lowered contents or activities of LDH, CK-MB, cTnI, IL-6, TNF-α, Cyt-C and MDA in the plasma (P<0.05), increased plasma SOD activity (P<0.05), reduced size of myocardial infarction, decreased myocardial expression of Bax and cleaved caspase-3 protein (P<0.05), and increased myocardial expression of Bcl-2 protein (P<0.05). All these changes induced by endomorphin-1 were obviously reversed by atractyloside postconditioning (P<0.05).

Conclusion: Endomorphin-1 postconditioning protects against myocardial IR injury in rats probably by inhibiting the opening of MPTP and reducing cardiac myocyte apoptosis via down-regulating cleaved caspase-3 expression.

Citing Articles

[PI3K/Akt signaling pathway mediates the protective effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats].

Wu S, Zhang L, Fan H, Huang Y, Zong Q, Gao Q Nan Fang Yi Ke Da Xue Xue Bao. 2021; 41(6):870-875.

PMID: 34238739 PMC: 8267992. DOI: 10.12122/j.issn.1673-4254.2021.06.09.

References

He Z, Peng Z, Jin L, Xu J, Chai X . Effect of morphine preconditioning on mitochondrial permeability transition pore after myocardial ischemia-reperfusion injury in rats. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010; 35(8):800-6. DOI: 10.3969/j.issn.1672-7347.2010.08.005. View

Laker R, Taddeo E, Akhtar Y, Zhang M, Hoehn K, Yan Z . The Mitochondrial Permeability Transition Pore Regulator Cyclophilin D Exhibits Tissue-Specific Control of Metabolic Homeostasis. PLoS One. 2016; 11(12):e0167910. PMC: 5179060. DOI: 10.1371/journal.pone.0167910. View

Zhang W, Zong Q, Gao Q, Yu Y, Gu X, Wang Y . Effects of endomorphin-1 postconditioning on myocardial ischemia/reperfusion injury and myocardial cell apoptosis in a rat model. Mol Med Rep. 2016; 14(4):3992-8. DOI: 10.3892/mmr.2016.5695. View

Xi J, Tian W, Zhang L, Jin Y, Xu Z . Morphine prevents the mitochondrial permeability transition pore opening through NO/cGMP/PKG/Zn2+/GSK-3beta signal pathway in cardiomyocytes. Am J Physiol Heart Circ Physiol. 2009; 298(2):H601-7. DOI: 10.1152/ajpheart.00453.2009. View

Shahzad T, Kasseckert S, Iraqi W, Johnson V, Schulz R, Schluter K . Mechanisms involved in postconditioning protection of cardiomyocytes against acute reperfusion injury. J Mol Cell Cardiol. 2013; 58:209-16. DOI: 10.1016/j.yjmcc.2013.01.003. View

De Marchi E, Bonora M, Giorgi C, Pinton P . The mitochondrial permeability transition pore is a dispensable element for mitochondrial calcium efflux. Cell Calcium. 2014; 56(1):1-13. PMC: 4074345. DOI: 10.1016/j.ceca.2014.03.004. View

Gomez-Crisostomo N, Lopez-Marure R, Zapata E, Zazueta C, Martinez-Abundis E . Bax induces cytochrome c release by multiple mechanisms in mitochondria from MCF7 cells. J Bioenerg Biomembr. 2013; 45(5):441-8. DOI: 10.1007/s10863-013-9508-x. View

Brenner D, Mak T . Mitochondrial cell death effectors. Curr Opin Cell Biol. 2009; 21(6):871-7. DOI: 10.1016/j.ceb.2009.09.004. View

Yao Y, Li L, Chen L, Wang W, Li L, Gao C . Sevoflurane postconditioning protects isolated rat hearts against ischemia-reperfusion injury: the role of radical oxygen species, extracellular signal-related kinases 1/2 and mitochondrial permeability transition pore. Mol Biol Rep. 2009; 37(5):2439-46. DOI: 10.1007/s11033-009-9755-4. View

10.

Harvey K, Hussain A, Maddock H . Ipratropium bromide-mediated myocardial injury in in vitro models of myocardial ischaemia/reperfusion. Toxicol Sci. 2014; 138(2):457-67. DOI: 10.1093/toxsci/kfu001. View

11.

Petrosillo G, Di Venosa N, Moro N, Colantuono G, Paradies V, Tiravanti E . In vivo hyperoxic preconditioning protects against rat-heart ischemia/reperfusion injury by inhibiting mitochondrial permeability transition pore opening and cytochrome c release. Free Radic Biol Med. 2010; 50(3):477-83. DOI: 10.1016/j.freeradbiomed.2010.11.030. View

12.

Obame F, Plin-Mercier C, Assaly R, Zini R, Dubois-Rande J, Berdeaux A . Cardioprotective effect of morphine and a blocker of glycogen synthase kinase 3 beta, SB216763 [3-(2,4-dichlorophenyl)-4(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione], via inhibition of the mitochondrial permeability transition pore. J Pharmacol Exp Ther. 2008; 326(1):252-8. DOI: 10.1124/jpet.108.138008. View

13.

Piper H, Meuter K, Schafer C . Cellular mechanisms of ischemia-reperfusion injury. Ann Thorac Surg. 2003; 75(2):S644-8. DOI: 10.1016/s0003-4975(02)04686-6. View

14.

Kroemer G, Reed J . Mitochondrial control of cell death. Nat Med. 2000; 6(5):513-9. DOI: 10.1038/74994. View

15.

Chen Z, Spahn D, Zhang X, Liu Y, Chu H, Liu Z . Morphine Postconditioning Protects Against Reperfusion Injury: the Role of Protein Kinase C-Epsilon, Extracellular Signal-Regulated Kinase 1/2 and Mitochondrial Permeability Transition Pores. Cell Physiol Biochem. 2016; 39(5):1930-1940. DOI: 10.1159/000447890. View

16.

Dorsch M, Behmenburg F, Raible M, Blase D, Grievink H, Hollmann M . Morphine-Induced Preconditioning: Involvement of Protein Kinase A and Mitochondrial Permeability Transition Pore. PLoS One. 2016; 11(3):e0151025. PMC: 4788451. DOI: 10.1371/journal.pone.0151025. View

17.

Lejay A, Fang F, John R, Van J, Barr M, Thaveau F . Ischemia reperfusion injury, ischemic conditioning and diabetes mellitus. J Mol Cell Cardiol. 2016; 91:11-22. DOI: 10.1016/j.yjmcc.2015.12.020. View

18.

Singh L, Pushker N, Saini N, Sen S, Sharma A, Bakhshi S . Expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins in human retinoblastoma. Clin Exp Ophthalmol. 2014; 43(3):259-67. DOI: 10.1111/ceo.12397. View

19.

Lindsay J, Degli Esposti M, Gilmore A . Bcl-2 proteins and mitochondria--specificity in membrane targeting for death. Biochim Biophys Acta. 2010; 1813(4):532-9. DOI: 10.1016/j.bbamcr.2010.10.017. View

20.

Zou H, Yang R, Hao J, Wang J, Sun C, Fesik S . Regulation of the Apaf-1/caspase-9 apoptosome by caspase-3 and XIAP. J Biol Chem. 2002; 278(10):8091-8. DOI: 10.1074/jbc.M204783200. View