Morphine Postconditioning alleviates autophage in ischemia-reperfusion induced cardiac injury through up-regulating lncRNA UCA1.

Abstract

Cardiac injury that induced by ischemia-reperfusion (I/R) significantly threatens human life, and autophagic cell death plays a pivotal role underlying it. Morphine Postconditioning (MpostC) has been identified to protect hearts against reperfusion injury, while whether MpostC treatment ameliorated cell autophage was still unclear. The I/R rats were induced using left anterior descending artery occlusion followed by reperfusion. The H9C2 cells were hypoxia/reoxygenation (H/R) treated to mimic I/R in vitro. Luciferase reporter assay was performed to verify the relationship between miR-128 and HSP70, while RNA immunoprecipitation (RIP) and RNA pull-down were conducted to determine the interaction between UCA1 and miR-128. The expression of UCA1, miR-128 and HSP70 was decreased, increased and decreased, individually, in I/R cardiac tissues, while MpostC treatments significantly reversed it and also ameliorated infarct size and cell autophage. UCA1 regulated the expression of miR-128, while miR-128 regulated HSP70. MpostC alleviated cell autophage and tissue infarct as well as reversed the expression of UCA1, while miR-128 and HSP70 that induced by I/R caused cardiac injury and H/R. The present study indicated that MpostC protected against cardiac injury that induced by I/R through regulating UCA1/miR-128/HSP70.