Abstract
ObjectivesDendrobium catenatum Lindl. (DH) is a Chinese herbal medicine, which is often used to make tea to improve immunity in China. Rumor has it that DH has a protective effect against cardiovascular disease. However, it is not clear how DH can prevent cardiovascular disease, such as atherosclerosis (AS). Therefore, the purpose of this study is to study whether DH can prevent AS and the underlying mechanisms. Methods Zebrafish larvae were fed with high-cholesterol diet (HCD) to establish a zebrafish AS model. Then, we used DH water extracts (DHWE) to pretreat AS zebrafish. The plaque formation was detected by HE, EVG, and oil red O staining. Neutrophil and macrophage counts were calculated to evaluate the inflammation level. Reactive oxygen species (ROS) activity, malondialdehyde (MDA) content, and superoxide dismutase (SOD) activity in zebrafish were measured to reflect oxidative stress. The cholesterol accumulation and the levels of lipid, triglyceride (TG), and total cholesterol (TC) were measured to reflect lipid metabolism disorder. Then, parallel flow chamber was utilized to establish a low shear stress- (LSS-) induced endothelial cell (EC) dysfunction model. EA.hy926 cells were exposed to LSS (3 dyn/cm2) for 30 min and treated with DHWE. The levels of ROS, SOD, MDA, glutathione (GSH), and glutathiol (GSSG) in EA.hy926 cells were analysed to determine oxidative stress. The release of nitric oxide (NO), endothelin-1 (ET-1), and epoprostenol (PGI2) in EA.hy926 cells was measured to reflect EC dysfunction. The mRNA expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in EA.hy926 cells was detected to reflect EC dysfunction inflammation. Results The results showed that DHWE significantly reduced cholesterol accumulation and macrophage infiltration in early AS. Finally, DHWE significantly alleviate the lipid metabolism disorder, oxidative stress, and inflammation to reduce the plaque formation of AS zebrafish larval model. Meanwhile, we also found that DHWE significantly improved LSS-induced EC dysfunction and oxidative stress in vitro. Conclusion Our results indicate that DHWE could be used as a prevention method to prevent AS.
Highlights
Atherosclerosis (AS) is characterized by endothelial dysfunction, inflammation, progressive lipid deposition, and vessel stiffness with potential complications, such as myocardial infarction or stroke [1, 2]
The plaques in the blood vessels of each group of zebrafish were detected by HE staining, EVG staining, and oil red O staining
There were no plaques were observed in the blood vessels of zebrafish in the control group (Figure 2)
Summary
Atherosclerosis (AS) is characterized by endothelial dysfunction, inflammation, progressive lipid deposition, and vessel stiffness with potential complications, such as myocardial infarction or stroke [1, 2]. Hypercholesterolemia is an important risk factor for the occurrence and development of AS. Hypercholesterolemia raises blood lipid levels, causing lipids to accumulate in blood vessels, forming early AS plaques [3]. Hypercholesterolemia can cause oxidative stress and inflammation and promote AS [4]. A force between blood flow and blood vessel endothelium for the unit area of the blood vessel wall, is mainly divided into low shear stress (LSS), high shear stress, laminar shear stress, and oscillation shear stress. LSS can Mediators of Inflammation induce endothelial cell (EC) dysfunction and oxidative stress, eventually leading to plaque formation [8, 9]. LSS promotes AS by priming ECs for enhanced expression of inflammatory molecules (e.g., intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule1 [VCAM-1]) [10]
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