Isolation of Prunin FromBauhinia variegataand Its Antioxidant Activity in Rats Fed an Atherogenic Diet

促炎细胞因子 抗氧化剂 内分泌学 内科学 硫代巴比妥酸 氧化应激 胆固醇 甘油三酯 化学 脂蛋白 肿瘤坏死因子α 过氧化氢酶 医学 药理学 炎症 生物化学 脂质过氧化
作者
Xi Zhang,Binghua Ye
出处
期刊:Natural Product Communications [SAGE Publishing]
卷期号:15 (10) 被引量:3
标识
DOI:10.1177/1934578x20967875
摘要

Atherosclerosis is no longer a disease attributed mainly to high cholesterol content in the body; it has come to be regarded as a chronic inflammatory disease with an autoimmune component. The purpose of this study was to investigate the effect of the prunin fraction (PF) isolated from the ethanolic extract of Bauhinia variegata against the release of various proinflammatory mediators in rats fed an atherogenic diet. The diet was administered orally to Sprague Dawley rats for 60 days to induce atherosclerosis. The blood serum of the rats was used to estimate the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), thiobarbituric acid reactive substance, catalase, total cholesterol, triglyceride, low-density lipoprotein, and high-density lipoprotein using assay kits. Other physical parameters, such as body weight, feed intake, and systolic blood pressure, were also determined during the study. The results showed a significant protective effect of the PF against diet-induced atherosclerosis by decreasing the levels of proinflammatory mediators such as TNF-α and IL-6. Rats treated with PF (20 and 40 mg/kg) showed a change in systolic blood pressure and a reduction in oxidative stress induced by the atherogenic diet. Reduction in body weight and modulation of food intake were observed in PF-treated rats, which indicated atheroprotective, hypolipidemic, and antioxidant effects. The study concludes that the atheroprotective properties of PF are due to effects on the initial phase of plaque formation to thrombus formation. This study may help researchers to find a better alternative for selecting optimal therapies and preventing plaque formation. Future Significance: This article focuses on the molecular mechanisms involved in the evolution of atherosclerotic plaques and different targets that act at the starting stage of the plaque to thrombus formation. This may pave the way for selecting optimal therapies and preventing plaque complications.
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