Abstract

Qingxuan Jiangya Decoction (QXJYD), a traditional Chinese medicine formula prescribed by academician Ke-ji Chen, has been used in China to clinically treat hypertension for decades of years. However, the molecular mechanisms of its action remain largely unknown. In this study, we examined the therapeutic efficacy of QXJYD against elevated systolic blood pressure in the spontaneously hypertensive rat (SHR) model, and investigated the underlying molecular mechanisms. We found that oral administration of QXJYD significantly reduced the elevation of systolic blood pressure in SHR but had no effect on body weight change. Additionally, QXJYD treatment significantly decreased the media thickness and ratio of media thickness/lumen diameter in the carotid arteries of SHR. Moreover, QXJYD remarkably promoted apoptosis of vascular smooth muscle cells and reduced the expression of anti-apoptotic B-cell leukemia/lymphoma 2. Furthermore, QXJYD significantly decreased the plasma Angiotensin II level in SHR. Collectively, our findings suggest that reversing vascular remodeling via inducing VSMC apoptosis could be one of the mechanisms whereby QXJYD treats hypertension.

Highlights

  • Hypertension is a key risk factor for various cardiovascular diseases, such as stroke, myocardial infarction, and heart failure [1], accounting for approximately 9.4 million deaths globally each year [2]

  • spontaneously hypertensive rat (SHR) model, in the present study we found that Qingxuan Jiangya Decoction (QXJYD) could significantly reduce elevated systolic the mechanism mediating the bioactivity of QXJYD, we evaluated its effect onTovascular remodeling

  • Our data showed that treatment could significantly decrease the media thickness mechanism mediating the bioactivity of QXJYD, we evaluated its effect on vascular remodeling. (MT)

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Summary

Introduction

Hypertension is a key risk factor for various cardiovascular diseases, such as stroke, myocardial infarction, and heart failure [1], accounting for approximately 9.4 million deaths globally each year [2]. Vascular remodeling is an early key outcome of hypertension, characterized by the hypertrophy of vascular smooth muscle cells (VSMCs) and Molecules 2016, 21, 956; doi:10.3390/molecules21070956 www.mdpi.com/journal/molecules. Vascular remodeling is initially an adaptive process in response to long-term pressure overload, it contributes to the pathophysiology of vascular diseases, circulatory disorders, and organ damage [4,5]. Increased vascular mass and arterial wall rigidity accompanied by VSMC hypertrophy of extracellular matrix [4]. Vascular remodeling initially an adaptive process in response or hyperplasia are key contributors to hypertension [9,10,11].isVascular remodeling is often characterized long-term between pressure overload, it contributes to the pathophysiology of vascular diseases, circulatory by an to imbalance proliferation and apoptosis in VSMCs [12]

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