Department of Biochemistry, University of Kerala, Thiruvananthapuram, Kerala, India.
Nutrition. 2013 Jan;29(1):219-29. doi: 10.1016/j.nut.2012.01.019. Epub 2012 May 15.
Recent advances have established a fundamental role for inflammation in mediating all stages of atherosclerosis, from initiation through progression. Quercetin may be a powerful bioactive constituent of the human diet, as a free radical scavenging agent and through interactions with various endogenous proteins. The present study focused on the effect of quercetin on inflammation induced by a hypercholesterolemic diet (HCD) in rabbits.
The animals were subjected to two different experiments, atherosclerotic progression and regression. In the atherosclerotic progression study, quercetin (25 mg/kg of body weight) was administered with the HCD for 90 d. In the atherosclerotic regression study, the animals were fed with the HCD for 90 d and then supplemented with quercetin (25 mg/kg of body weight) for another 90 d. The inflammatory enzyme activities were examined and a histopathologic examination of the aorta was performed.
In the atherosclerotic progression study, quercetin coadministered with the HCD significantly decreased the activities of inflammatory enzymes such as cyclooxygenase, lipoxygenases (LOX) such as 5-LOX and 12-LOX in monocytes, nitric oxide synthase activity in the plasma, myeloperoxidase activity in the aorta, and the level of C-reactive protein in serum. In the regression study, quercetin administration significantly decreased the increased activities of inflammatory mediators such as cyclooxygenase, 5-LOX, 12-LOX, myeloperoxidase, and nitric oxide synthase and the serum level of C-reactive protein in HCD-fed rabbits compared with regression control rabbits. This effect was confirmed by histopathologic examination of the aorta.
This study demonstrates that quercetin modulates the deleterious inflammatory effects induced by an HCD in vivo in rabbits, suggesting its beneficial effect in decreasing inflammation in atherosclerotic progression and regression.
最近的研究进展确立了炎症在介导动脉粥样硬化的所有阶段(从起始到进展)中的基本作用。槲皮素可能是人类饮食中的一种强大的生物活性成分,它可以作为自由基清除剂,并通过与各种内源性蛋白质相互作用发挥作用。本研究集中于槲皮素对高胆固醇饮食(HCD)诱导的兔炎症的影响。
动物进行了两项不同的实验,动脉粥样硬化的进展和消退。在动脉粥样硬化进展研究中,HCD 喂养 90 天时给予槲皮素(25mg/kg 体重)。在动脉粥样硬化消退研究中,动物用 HCD 喂养 90 天,然后再补充槲皮素(25mg/kg 体重)90 天。检查炎症酶活性,并对主动脉进行组织病理学检查。
在动脉粥样硬化进展研究中,HCD 与槲皮素联合使用可显著降低炎症酶如环加氧酶、单核细胞中脂加氧酶(如 5-LOX 和 12-LOX)、血浆中一氧化氮合酶活性、主动脉中髓过氧化物酶活性和血清中 C-反应蛋白水平。在消退研究中,与消退对照组相比,槲皮素给药可显著降低 HCD 喂养兔中炎症介质如环加氧酶、5-LOX、12-LOX、髓过氧化物酶和一氧化氮合酶的活性增加以及血清中 C-反应蛋白的水平。主动脉的组织病理学检查证实了这一效果。
本研究表明,槲皮素调节 HCD 体内诱导的有害炎症作用,提示其在减少动脉粥样硬化进展和消退中的炎症有益作用。