Protective Effects Of Luteolin On Vascular Endothelial Injury In Rats With Atherosclerosis

Objective: The incidence and mortality of atherosclerotic vascular diseases are increasing year by year. The preferred lipid-regulating drugs are statins, which may have potential risk of diseases such as myositis, diabetes, cataract, etc. This study aimed to investigate the protective effects of luteolin on vascular endothelial injury in rats with atherosclerosis. Methods: An atherosclerosis model was established in SD rats. Then, the rats were randomly divided into model group and 20, 40 and 80 mg/kg luteolin groups (12 rats in each group), and were intra-gastrically administrated with normal saline, 20, 40 and 80 mg/kg luteolin, respectively. The rats in the control group (12 rats) were fed with normal saline. After treatment for 6 weeks, the hemodynamic indexes, blood indexes, and aortic tissue adhesion factors of rats were determined. Results: After treatment, compared with the model group, the serum total cholesterol, triglyceride and low-density lipoprotein levels in 40 and 80 mg/kg luteolin groups were decreased while the serum high-density lipoprotein level was increased. Furthermore, the maximum rate of left ventricular pressure rise (dp/dt(max)) was increased, and the time from onset of contraction to dp/dt(max) was decreased. The serum tumor necrosis factor alpha, interleukin 6 and C-reactive protein levels were decreased and the serum superoxide dismutase and glutathione peroxidase levels were increased. Serum malondialdehyde level was decreased and the serum endothelin level was decreased. Likewise, the serum nitric oxide level was increased and the aortic tissue intercellular cell adhesion molecule 1 and vascular cell adhesion molecule 1 levels were decreased (all P < 0.05). Conclusions: Luteolin can mitigate the vascular endothelial injury in atherosclerosis rats. The mechanisms may be related to its resistance of inflammatory response and oxidative stress and regulation of expressions of vasoconstriction and vasodilatation factors and aortic tissue adhesion factors.