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Hui-hua Chen [1] and Pei Zhao [2] and Jing Tian [1] and Wei Guo [1] and Ming Xu [3] and Chen Zhang [1] and Rong Lu [1]

Academic Editor: Settimio Grimaldi

1, Department of Pathology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China, shutcm.edu.cn

2, Public Experiment Platform, School of Basic Medical Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China, shutcm.edu.cn

3, Department of Physiology, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China, shutcm.edu.cn

Received Feb 11, 2017; Accepted Jun 13, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Pressure overload imposes hemodynamic burden on the left ventricle (LV), which initiates a series of events leading to ventricular remodeling, including hypertrophy (LVH) and fibrosis, and eventually heart failure. Although in the early stages LVH may seem to be an adaptive phenomenon, it has been recognized as an independent risk factor for cardiovascular morbidity and mortality, including heart failure [1]. Pressure overload-induced LVH is accompanied by the accumulation of collagen in the extracellular matrix, which alters myocardial stiffness and consequently affects cardiac function [2]. Recently, emerging evidences demonstrated that hypertrophied heart is accompanied by proliferating of cardiac microtubules and altered the posttranslational modifications (PTMs) on tubulin, such as detyrosination and acetylation of tubulin [3].

Guizhi Gancao Decoction (GGD), which consists of Guizhi (Cinnamomum cassia Presl.) and Gancao (Glycyrrhiza uralensis), was originally described in Han dynasty. It has been widely used for therapy against cardiovascular diseases in China for thousands years. Modern pharmacological studies have revealed serval bioactive constituents of GGD that may have cardioprotective effects. Yang et al. reported that Cinnmaldehyde attenuates aortic banding induced cardiac hypertrophy and fibrosis probably via blocking ERK signaling pathway [4]. Du et al. demonstrated that glycyrrhizin and some of its derivatives treat heart failure by inhibiting High-Mobility Group Box 1 [5]. Parisella et al. have revealed that glycyrrhizin has positive inotropic and lusitropic effects which were negatively affected by glycyrrhetinic acid. They also found that glycyrrhizin acts through the endothelin receptor type A/phospholipase C axis, while glycyrrhetinic acid acts through endothelin receptor type B/Akt/nitric oxide synthase/nitric oxide axis...

    

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