Na Yan,1 Xianggui Wang,1 Zufang Xu,1 Linling Zhong,1 Jiangyong Yang2 

1Department of Vasculocardiology, Ganzhou People’s Hospital, Ganzhou, People’s Republic of China; 2Department of Cardiology, Ganzhou Hospital of Guangdong Provincial People’s Hospital, Ganzhou Municipal Hospital, Ganzhou, People’s Republic of China

Correspondence: Jiangyong Yang, Department of Cardiology, Ganzhou Hospital of Guangdong Provincial People’s Hospital, Ganzhou Municipal Hospital, No. 49, Dagong Road, Ganzhou, 341000, People’s Republic of China, Tel +86-797-8208553, Email yangjy19861208@163.com

Introduction: Apigenin is a natural flavonoid compound with promising potential for the attenuation of myocardial hypertrophy (MH). The compound can also modulate the expression of miR-185-5p that both promote MH and suppress autophagy. The current attempts to explain the anti-MH effect of apigenin by focusing on changes in miR-185-5p-mediated autophagy.
Methods: Hypertrophic symptoms were induced in rats using transverse aortic constriction (TAC) method and in cardiomyocytes using Ang II and then handled with apigenin. Changes in myocardial function and structure and cell viability and surface area were measured. The role of miR-185-5p in the anti-MH function of apigenin was explored by detecting changes in autophagic processes and miR-185-5p/SREBP2 axis.
Results: TAC surgery induced weight increase, structure destruction, and collagen deposition in hearts of model rats. Ang II suppresses cardiomyocyte viability and increased cell surface area. All these impairments were attenuated by apigenin and were associated with the restored level of autophagy. At the molecular level, the expression of miR-185-5p was up-regulated by TAC, while the expression of SREBP2 was down-regulated, which was reserved by apigenin both in vivo and in vitro. The induction of miR-185-5p in cardiomyocytes could counteracted the protective effects of apigenin.
Discussion: Collectively, the findings outlined in the current study highlighted that apigenin showed anti-MH effects. The effects were related to the inhibition of miR-185-5p and activation of SREBP, which contributed to the increased autophagy.

Keywords: apigenin, autophagy, miR-185-5p, myocardial hypertrophy, SREBP2