Could omega-3 fatty acids preserve endothelial function in a rat model of rheumatoid arthritis?

Eman A Allam, E. Omar
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Abstract

Could omega-3 fatty acids preserve endothelial function in a rat model of rheumatoid arthritis? Background: Endothelial dysfunction is claimed to be the cause of increased risk for cardiovascular diseases in rheumatoid arthritis (RA) patients. Omega-3 fatty acids is a promising drug in this field; however, its exact effects on endothelial functions are not fully understood. Aim of the work: This study aimed to evaluate the effect of omega-3 fatty acids on endothelial reactivity and some markers of endothelial dysfunction [Vascular cell adhesion molecule-1 (VCAM-1), tumour necrosis factor alpha (TNF-α), Malondialdehyde (MDA) and NOS activity] in a rat model of rheumatoid arthritis. Material & methods: Thirty male rats were divided into 3 groups (control, untreated RA, and RA group with omega-3 supplementation). RA induction was done by intradermal injection of heat-killed Mycobacterium butyricum and was confirmed by clinical signs of arthritis on day 11. In the treated group, omega-3 was given daily via gastric gavage starting from day 11 until the end of the study. The study duration was 30 days for all groups starting from the day of induction. At the end of the study, rats were sacrificed, blood samples were collected for VACM-1, TNF-α, MDA and nitrite measurement and thoracic aortae were taken to test vascular reactivity. Results: All markers increased while vascular reactivity decreased significantly after RA induction. Omega-3 treatment significantly decreased all biochemical markers and restored normal vascular reactivity in the treated group.
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欧米茄-3脂肪酸能保护类风湿关节炎大鼠模型的内皮功能吗?
欧米茄-3脂肪酸能保护类风湿关节炎大鼠模型的内皮功能吗?背景:内皮功能障碍被认为是类风湿关节炎(RA)患者心血管疾病风险增加的原因。欧米伽-3脂肪酸在这个领域是很有前途的药物;然而,其对内皮功能的确切影响尚不完全清楚。工作目的:本研究旨在评估omega-3脂肪酸对类风湿关节炎大鼠模型内皮反应性和内皮功能障碍的一些标志物[血管细胞粘附分子-1 (VCAM-1),肿瘤坏死因子α (TNF-α),丙二醛(MDA)和NOS活性]的影响。材料与方法:30只雄性大鼠分为3组(对照组、未治疗组和补充omega-3组)。采用热杀丁酸分枝杆菌皮内注射诱导RA,第11天出现关节炎临床症状。在治疗组中,从第11天开始,每天通过胃灌胃给予omega-3,直到研究结束。自诱导之日起,各组试验持续30 d。实验结束时,处死大鼠,采血测定VACM-1、TNF-α、MDA和亚硝酸盐含量,取胸主动脉检测血管反应性。结果:RA诱导后各指标均升高,血管反应性明显降低。Omega-3治疗显著降低了治疗组的所有生化指标,恢复了正常的血管反应性。
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