pPolyHb protects myocardial H9C2 cells against ischemia-reperfusion injury by regulating the Pink1-Parkin-mediated mitochondrial autophagy pathway

Abstract

Mitochondrial dysfunction is a major contributory factor for myocardial ischemia-reperfusion (I/R) injury. It has been reported that Pink1-Parkin-mediated mitochondrial autophagy could effectively remove damaged mitochondria and excess ROS to ensure the stability of intracellular mitochondria. The present study was designed to evaluate whether the polymerized porcine haemoglobin (pPolyHb), a novel type of haemoglobin oxygen carrier, has an effect on I/R injury via regulating the Pink1-Parkin mediated mitochondrial autophagy pathway in myocardial H9C2 cells. The results revealed that pPolyHb could effectively reduce apoptosis and improve the survival rates of H9C2 cells. In addition, Pink1 and Parkin levels gradually decreased with pPolyHb reoxygenation. The inhibition of mitochondrial autophagy through mitochondrial-division inhibitor-1(mdivi-1) resulted in a decrease in anti-apoptotic protein Bcl-2 and an increase in pro-apoptotic protein Bax and CytC. In conclusion, pPolyHb has a protective effect on myocardial ischemia-reperfusion injury by regulating moderate mitochondrial autophagy.

Keywords:

• Polymerized porcine haemoglobin (pPolyHb)
• ischemia-reperfusion injury
• mitochondrial autophagy
• Pink1-Parkin

Acknowledgements

We would like to thank LetPub (www.letpub.com) for providing linguistic assistance during the preparation of this manuscript.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the National Key R&D Program of China [grant nos. 2018YFC1106500]. National Science and Technology Major Projects for Major New Drugs Innovation and Development [Grant No: 2019ZX09J19101 and 2014ZX09102043-004]. National Natural Science Foundation of China [Program Number: 81102367]. We also acknowledge with thanks the grants from Shanxi Science and Technology Department [grant nos. 2016SF-243, 2011KTCL03-23 and 2011K12-03–10].