Abstract
Gentianella acuta (G. acuta) has been widely used as a traditional medicine by Chinese Mongolian populations for the treatment of heart diseases and has also been tested in modern pharmacological experiments. However, the effects of G. acuta on cardiovascular damage and inflammation under conditions of hypercholesterolaemia remain unclear. The present study investigated the effects and mechanisms of the water extract of G. acuta on cardiovascular damage and inflammation caused by a high-cholesterol diet. Male Sprague-Dawley rats were fed a high-cholesterol diet for 4 weeks to establish the hypercholesterolaemia rat model, and they were administered physiological saline or 1.2 g/kg of G. acuta by gavage starting from the 15th day. After the last administration, the blood, heart and thoracic aorta samples were collected and examined. It was revealed that G. acuta treatment could ameliorate cardiomyocyte disorder and thoracic aortic vessel wall damage, reduce serum lipid levels and inflammatory factors and improve heart function. Compared with the Model group, the serum levels of triglycerides, total cholesterol, low-density lipoprotein and tumour necrosis factor-α were decreased, and the high-density lipoprotein and interleukin-10 levels were increased in the Model-G group. Moreover, in both the heart and thoracic aorta, G. acuta reduced the expression and phosphorylation of inhibitor of nuclear factor kappa-B kinase β (IKKβ), inhibitor of NF-κB-α (IκBα) and p-nuclear factor kappa-B (NF-κB). Therefore, G. acuta may exert an inhibitory effect on the IKK/IκB/NF-κB signalling pathway to protect the heart and thoracic aorta in hypercholesterolaemic rats.
Highlights
Cardiovascular disease (CVD) is an important health concern and has been the focus of considerable research
The levels of TG, total cholesterol (TC) and low‐density lipoprotein (LDL) were significantly decreased, and those of high‐density lipoprotein (HDL) were significantly increased in the Model‐G group compared with those in the Model group (Fig. 1; P
Compared with the Model group, tumour necrosis factor‐α (TNF‐α) was significantly decreased in the Model‐G group (P
Summary
Cardiovascular disease (CVD) is an important health concern and has been the focus of considerable research. Atherosclerosis (AS) is a major cause of CVD and the result of several factors, among which lipid metabolism disorders are the leading contributor. Lipid metabolism disorders are caused by hypercholesterolaemia and induce an inflammatory response that is involved in all processes of AS [2,3]. The nuclear tran‐ scription factor controlling their release is phosphorylated (p)‐nuclear factor κB (NF‐κB), which has been revealed to induce an increase in the production of inflammatory and adhesion factors [4,5,6]. NF‐κB and the inhibitory protein inhibitor of NF‐κB‐α (IκBα) exist as a complex and are inactive. Numerous studies have reported that oxidative stress is an important cause of AS and is closely associated with NF‐κB [11,12,13]. The occurrence of AS is closely linked to the IKK/IκB/NF‐κB pathway
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