Total Flavonoids from Carya cathayensis Sarg. Leaves Alleviate H9c2 Cells Hypoxia/Reoxygenation Injury via Effects on miR-21 Expression, PTEN/Akt, and the Bcl-2/Bax Pathway.

Ruibin Jiang,Zhishan Ding,Chengxian Gao,Nipi Chen,Bo Jin,Yan Guo

doi:10.1155/2018/8617314

Abstract

This study aimed to investigate whether the total flavonoids (TFs) from Carya cathayensis Sarg. leaves alleviate hypoxia/reoxygenation (H/R) injury in H9c2 cardiomyocytes and to explore potential mechanisms. H9c2 cells pretreated with TFs for 24h were exposed to H/R treatment. The results indicated that TFs significantly alleviate H/R injury, which include inhibiting apoptosis and enhancing antioxidant capacity. The protective effects of TFs resulted in higher expression of miR-21 in H/R-induced H9c2 cells than that of controls, which in turn upregulated Akt signaling activity via suppressing the expression of PTEN together with decreasing the ratio of Bax/Bcl-2, caspase3, and cleaved-caspase3 expression in H/R-induced H9c2 cells. Conversely, blocking miR-21 expression with miR-21 inhibitor effectively suppressed the protective effects of TFs against H/R-induced injury. Our study suggests that TFs can decrease cell apoptosis, which may be mediated by altering the expression of miR-21, PTEN/Akt, and Bcl/Bax.

Highlights

Cardiac ischemia/reperfusion (I/R) injury is a serious disease and threatens human health [1]
H9c2 cells were exposed to 10mM Na2S2O4 for 7h followed by reoxygenation for another 12h, and the results revealed that H/R injury resulted in decreasing cells viability
total flavonoids (TFs) pretreatment reversed the viability of H9c2 cells after H/R injury (Figure 2)

Summary

Introduction

Cardiac ischemia/reperfusion (I/R) injury is a serious disease and threatens human health [1]. Reperfusion treatment has a potential risk of worsening tissue damage after ischemia, which can accelerate the deterioration of cardiac function [2]. MiRNAs have been implicated as transcriptional regulators in a wide range of biological processes determining cell fate, stress response, proliferation, or death [5]. In murine cardiomyocytes miR-21 was found to protect from hypoxia/reoxygenation (H/R)-induced cell apoptosis via regulation of its target gene PDCD4 [13]. Despite the recent surge about miRNA discoveries for cardiac I/R injury, there is still very little known about the mechanism details because of the complexity of cellular events and the interference of other risk factors

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