Morphine Postconditioning alleviates autophage in ischemia-reperfusion induced cardiac injury through up-regulating lncRNA UCA1 - 13/11/18
, Ruishan Liu c, Qingxiao Niu b, Han Wang b, Zhenkai Yang b, Yongxin Bao bBienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Background |
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.
Methods |
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.
Results |
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.
Conclusion |
The present study indicated that MpostC protected against cardiac injury that induced by I/R through regulating UCA1/miR-128/HSP70.
Le texte complet de cet article est disponible en PDF.Keywords : Morphine Postconditioning, Autophage, UCA1, Ischemia-reperfusion
Plan
Vol 108
P. 1357-1364 - décembre 2018 Retour au numéro
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