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Abstract
The Chinese medicinal formula Guanxin Shutong capsule (GXSTC) has been used for almost 10 years as a clinical treatment for chest pain, depression, palpitation and cardiovascular diseases. The aim of this study was to investigate the effects of GXSTC drug-containing serum on tumor necrosis factor-α (TNF-α)-stimulated endothelial cells. Cell viability was measured by MTT assay, and nitric oxide (NO) levels and NO synthase (NOS) activity were measured as standards of endothelial dysfunction. Malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were evaluated using commercial kits. In addition, the protein expression of endothelial NOS (eNOS), AKT and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits was examined to evaluate the effect of GXSTC drug-containing serum on ECV304 cells. GXSTC significantly reversed the decrease in NO production induced by TNF-α (5 ng/ml) in ECV304 cells. The expression of NADPH oxidase subunits was increased by TNF-α treatment, but markedly inhibited by treatment with GXSTC in TNF-α-stimulated cells. In summary, GXSTC increased the production of NO in ECV304 cells and exerted a protective effect on ECV304 cells stimulated with TNF-α by upregulating the mRNA and protein expression of eNOS. This was accompanied by increased SOD activity and reduced MDA levels. These results suggested that GXSTC protects the endothelium via the NO pathway and exhibits antioxidant effects.
Highlights
Cardiovascular disease (CVD) constitutes the leading cause of mortality worldwide
The concentration of 5 ng/ml tumor necrosis factor‐α (TNF‐α) was selected as an in vitro endothelial dysfunction model (Fig. 1A), and Guanxin Shutong capsule (GXSTC) increased the level of nitric oxide (NO) in a dose‐dependent manner in TNF‐α‐stimulated ECV304 cells (Fig. 1B)
TNF‐α stimulation resulted in reduced cell viability and increased the release of lactate dehydrogenase (LDH) and the lipid peroxidation product MDA; this was associated with increased production of NO and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, suggesting that underproduction of NO and downregulation of p-endothelial NOS (eNOS) may have partially mediated the cell death through enhancing oxidative stress and increasing the cellular lipid peroxidation
Summary
The major modifiable risk factors for ischemic heart disease principally include high blood pressure, high total cholesterol and low‐density lipoprotein cholesterol, low high‐density lipoprotein cholesterol, tobacco use, physical inactivity, poor nutrition and obesity. All of these established risk factors are known to cause endothelial activation and dysfunction [1,2]. Oxidative stress is a molecular dysregulation associated with reactive oxygen species (ROS) metabolism, and is a crucial factor in the pathogenesis of endothelial dysfunction, vascular inflammation and atherosclerosis [3]. TNF‐α has been shown to stimulate the upregulation of NO synthase (NOS) activity and NO production in ECV304 cells, which may be accompanied by a burst in production of intracellular ROS, including superoxide anion (O2‐) and hydrogen peroxide [5]
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