在胆固醇诱导的动脉粥样硬化中,补充富生育三烯醇混合组分后,体内c反应蛋白主动脉组织表达降低

N. A. Muhammad, E. Omar, H. Nawawi
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引用次数: 2

摘要

动脉粥样硬化是心血管疾病背后的潜在病理,是世界范围内死亡的主要原因。炎症在其发病机制中起关键作用。生育三烯醇是一种棕榈衍生的维生素E成分,已知具有有效的抗炎特性。生育三烯醇对动脉粥样硬化形成和发展的影响尚不清楚。目的:探讨富生育三烯醇混合组分(TEMF)对高胆固醇血症家兔的抗炎和抗动脉粥样硬化作用。方法:将20只新西兰大白兔随机分为2组,分别饲喂1%高胆固醇饲料(HCD) 2周(A组)和8周(B组),然后随机分为TEMF (15mg/kg)和安慰剂组(ii)。8周治疗期间,各组均给予正常饮食。对动脉粥样硬化病变进行分析,同时用免疫组织化学方法评估炎症的表达。结果:A组和b组经TEMF治疗后,动脉粥样硬化病变均无明显减少。然而,与安慰剂相比,TEMF中CRP阳性组织表达明显降低(3.01±0.86∶25.51±10.85%;p=0.05)和SMA(3.91±1.33∶16.19±4.08%;P =0.04)。此外,在A组和B组中,TEMF与安慰剂在NFκB、IL-6、ICAM-1、e -选择素和MMP-12方面均无显著差异。结论:TEMF治疗8周对早期和重度动脉粥样硬化病变均有中性作用。然而,TEMF治疗降低了主动脉内膜组织CRP的表达,特别是在早期动脉粥样硬化中,表明其在体内具有抗炎作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reduced in-vivo C-reactive protein aortic tissue expression following tocotrienol-enriched mixed fraction supplementation in cholesterol-induced atherosclerosis
Atherosclerosis is the underlying pathology behind cardiovascular disease, the main cause of death in worldwide. Inflammation plays a pivotal role in its pathogenesis. Tocotrienol is a palm derived vitamin E component, known have potent anti-inflammatory properties. The effect of tocotrienol on formation and progression of atherosclerosis is unknown. Aim: to determine the anti-inflammatory and anti-atherosclerotic effects of tocotrienol-enriched mixed fraction (TEMF) supplementation in hypercholesterolaemia induced rabbits. Methods: 20 New Zealand white rabbits were randomised into two groups and fed with 1% high cholesterol diet (HCD) for (i) 2 weeks in group A and (ii) 8 weeks in group B, followed by randomization into two treatment groups: (i) TEMF (15mg/kg) or (ii) placebo for 8 weeks. During the 8 week treatment duration, all the groups were given normal diet. Analyses of atherosclerotic lesions were performed while expression of inflammatory was evaluated using immunohistochemistry. Results: There were no significant reduction in atherosclerotic lesions with TEMF treatment for both groups A and B. However, there were significantly lower positive tissue expression in TEMF compared to placebo for CRP (3.01 ± 0.86 vs. 25.51 ± 10.85%; p=0.05) and SMA (3.91 ± 1.33 vs. 16.19 ± 4.08%; p=0.04) in early atherosclerosis. In addition, no significant differences were observed between TEMF and placebo in both groups A and B for NFκB, IL-6, ICAM-1, E-selectin and MMP-12. Conclusion: Eight weeks treatment with TEMF has neutral effects on atherosclerotic lesions in both early and severe atherosclerosis. However, TEMF treatment reduces aortic intimal tissue expression of CRP especially in early atherosclerosis indicating its in vivo anti-inflammatory effects.
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