Matrine regulates H2O2-induced oxidative stress through long non-coding RNA HOTAIR/miR-106b-5p axis via AKT and STAT3 pathways.

Matrine is a main active constituent of Chinese herb Sophora flavescens Ait (Kushen), which has shown various pharmacological effects, and has been reported to exhibit protective effects in heart failure. In the present study, the underlying mechanism of matrine was explored in H2O2-induced H9c2 cell line. It was confirmed that matrine could alleviate H2O2-induced injury in H9c2 cells. And the down-regulation of long non-coding RNA HOTAIR induced by H2O2 could be reversed by treating with matrine. Moreover, overexpression of HOTAIR promoted cell viability and superoxide dismutase (SOD) level, but inhibited cell apoptosis and lactate dehydrogenase (LDH) level. We found that miR-106b-5p was a target of HOTAIR and negatively regulated by HOTAIR. Moreover, up-regulation of miR-106b-5p restored the effects of HOTAIR overexpression on cell viability, apoptosis, and the levels of LDH and SOD. In addition, matrine protected H9c2 cells from H2O2-induced injury through HOTAIR/miR-106b-5p axis. Furthermore, we discovered that matrine exerted protective effects on H2O2-induced H9c2 cells through activating STAT3 and AKT pathway. In brief, matrine modulated H2O2-induced myocardial oxidative stress repair through HOTAIR/miR-106b-5p axis via AKT and STAT3 signaling pathway. Our study may provide a therapeutic target for the therapy of oxidative stress heart diseases.