Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN

This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia–reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treat...

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Veröffentlicht in:Journal of biochemical and molecular toxicology 2022-10, Vol.36 (10), p.e23175-n/a
Hauptverfasser: Wei, Yuan, Xiao, Liang, Yingying, Liu, Haichen, Wang
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Sprache:eng
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Zusammenfassung:This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia–reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)‐induced H9c2 cardiomyocytes were used to establish an in‐vitro ischemia–reperfusion injury model of cardiomyocytes. Cells were treated with 1 μmol/L of PDG. Reactive oxygen species (ROS) level was detected by a 2′,7′‐dichlorofluorescein‐diacetate assay. The release of lactate dehydrogenase (LDH) and creatine kinase‐MB (CK‐MB) was examined by enzyme‐linked immunosorbent assay. The viability and apoptosis of H9c2 cells were probed by MTT assay and flow cytometry. Besides this, Western blot and quantitative real‐time PCR were used to detect microRNA‐142‐3p (miR‐142‐3p) and hypoxia‐inducible factor 1 subunit alpha inhibitor (HIF1AN) expression levels. The binding sequence between miR‐142‐3p and HIF1AN 3′‐untranslated region was validated by a dual‐luciferase reporter gene assay. PDG treatment significantly reduced the level of ROS, LDH, and CK‐MB, promoted viability, and inhibited the apoptosis of H9c2 cells. PDG treatment promoted miR‐142‐3p expression and inhibited HIF1AN expression in H9c2 cells. MiR‐142‐3p overexpression enhanced the effects of PDG on ROS, LDH, CK‐MB levels, cell viability, and apoptosis in H9c2 cardiomyocytes, while overexpression of HIF1AN reversed the above effects. PDG ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN.
ISSN:1095-6670
1099-0461
DOI:10.1002/jbt.23175