miR‑320‑3p is involved in morphine pre‑conditioning to protect rat cardiomyocytes from ischemia/reperfusion injury through targeting Akt3

Abstract

Morphine pre-conditioning (MPc) can significantly reduce myocardial ischemic injury and inhibit cardiomyocyte apoptosis, but the underlying mechanism still remains unclear. The aim of the present study was to investigate the protective mechanism of MPc in myocardial hypoxia/reoxygenation (H/r) injury at the microrna (mir) level. H9c2 cells were used as a model of H/r and subjected to morphine pre-treatment. The protective effects of MPc on H/r injury in cardiomyocytes were evaluated using MTT and colorimetric assay, as well as flow cytometry. In addition, reverse transcription-quantitative Pcr, western blotting and dual-luciferase reporter assay experiments were performed to determine the relationship between MPc, mir-320-3p and akt3, and their effects on H/r injury. The present study demonstrated that MPc enhanced cell activity, decreased ldH content, and reduced apoptosis in rat cardiomyocytes, suggesting that MPc could protect these cells from H/r injury. Moreover, MPc partially reversed the increase in mir-320-3p expression and the decrease in akt3 levels caused by H/r injury. inhibition of mir-320-3p expression also attenuated the effects of H/r on cardiomyocyte activity, ldH content and apoptosis. Furthermore, akt3 was predicted to be a target gene of mir-320-3p, and overexpression of mir-320-3p inhibited the expression of akt3, blocking the protective effects of MPc on the cells. The current findings revealed that MPC could protect cardiomyocytes from H/r damage through targeting mir-320-3p to regulate the Pi3K/akt3 signaling pathway. miR-320-3p is involved in morphine pre-conditioning to protect rat cardiomyocytes from ischemia/reperfusion injury through targeting Akt3lan cao 1 and SHiJun cHai 2 departments of 1 anesthesiology and

Clinical value of serum miR‐320‐3p expression in predicting the prognosis of sepsis‐induced acute kidney injury

“…Previous research on miR-320-3p has focused on pulmonary hypertension, ischaemia/reperfusion injury and muscle wasting in obesity. [10][11][12] In this study, the death group showed greatly higher the levels of serum miR-320-3p, NGAL, KIM-1 and the APACHE II mark than the survival group, suggesting that the levels of serum miR-320-3p, NGAL and KIM-1 are related to the severity of sepsis complicated with AKI, and may take part in the appearance and growth of AKI. Similarly, Hu X M et al displayed that serum NGAL and KIM-1 extents were significantly grown in the death group, and the combined detection of the two tests had good predictive value for neonatal renal injury with sepsis at 28d.…”

“…As far as we know, this is the first study which investigates miR‐320‐3p expression in AKI. Previous research on miR‐320‐3p has focused on pulmonary hypertension, ischaemia/reperfusion injury and muscle wasting in obesity 10–12 . In this study, the death group showed greatly higher the levels of serum miR‐320‐3p, NGAL, KIM‐1 and the APACHE II mark than the survival group, suggesting that the levels of serum miR‐320‐3p, NGAL and KIM‐1 are related to the severity of sepsis complicated with AKI, and may take part in the appearance and growth of AKI.…”

Micro‐RNA gene expressions during cardiopulmonary bypass

“…In the reported literature, in an experimentally induced ischemia/reperfusion model, higher miRNA‐320 levels were detected and reduced myocardial tissue damage was obtained by administration of miRNA‐320 anti‐miRNA‐320 45 . In another experimental study, it was shown that overexpression of miR‐320‐3p inhibited the protective pathways against ischemic injury on the myocardium 46 . Similarly, other ex vivo and in vivo studies demonstrated that miR‐320 has a regulatory role in ischemia reperfusion‐induced cardiac injury and dysfunction by the antithetical effect to heat‐shock protein 20 (Hsp20).…”

Analysis of miRNAs Involved in Mouse Heart Injury Upon Coxsackievirus A2 Infection

“…MiR-296-3p and miR-24-2-5p are important for embryonic stem (ES) cell (ESC) cardiac differentiation (Sun et al, 2011;Lee et al, 2016). MiR-320-3p can protect rat cardiomyocytes from ischemia/reperfusion (HR) injury through targeting Akt3 (Cao and Chai, 2020). MiR-30e-3p is involved in promoting cardiomyocyte autophagy and inhibiting apoptosis by regulating Egr-1 (Su et al, 2020).…”