低剂量阿司匹林（乙酰水杨酸）可防止9月龄HIV-1转基因大鼠（一种HIV-1相关神经认知障碍模型）大脑中前列腺素E2、15-表-脂氧素A4和8-异前列腺素浓度升高。
Low-dose aspirin (acetylsalicylate) prevents increases in brain PGE2, 15-epi-lipoxin A4 and 8-isoprostane concentrations in 9 month-old HIV-1 transgenic rats, a model for HIV-1 associated neurocognitive disorders.
作者信息
Blanchard Helene C, Taha Ameer Y, Rapoport Stanley I, Yuan Zhi-Xin
机构信息
Brain Physiology and Metabolism Section, Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
Brain Physiology and Metabolism Section, Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
出版信息
Prostaglandins Leukot Essent Fatty Acids. 2015 May;96:25-30. doi: 10.1016/j.plefa.2015.01.002. Epub 2015 Jan 13.
BACKGROUND
Older human immunodeficiency virus (HIV)-1 transgenic rats are a model for HIV-1 associated neurocognitive disorders (HAND). They show behavioral changes, neuroinflammation, neuronal loss, and increased brain arachidonic acid (AA) enzymes. Aspirin (acetylsalicylate, ASA) inhibits AA oxidation by cyclooxygenase (COX)-1 and COX-2.
HYPOTHESIS
Chronic low-dose ASA will downregulate brain AA metabolism in HIV-1 transgenic rats.
METHODS
Nine month-old HIV-1 transgenic and wildtype rats were given 42 days of 10mg/kg/day ASA or nothing in drinking water; eicosanoids were measured using ELISAs on microwaved brain extracts.
RESULTS
Brain 15-epi-lipoxin A4 and 8-isoprostane concentrations were significantly higher in HIV-1 transgenic than wildtype rats; these differences were prevented by ASA. ASA reduced prostaglandin E2 and leukotriene B4 concentrations in HIV-1 Tg but not wildtype rats. Thromboxane B2, 15-HETE, lipoxin A4 and resolvin D1 concentrations were unaffected by genotype or treatment.
CONCLUSION
Chronic low-dose ASA reduces AA-metabolite markers of neuroinflammation and oxidative stress in a rat model for HAND.
背景
老年人类免疫缺陷病毒（HIV）-1转基因大鼠是HIV-1相关神经认知障碍（HAND）的一种模型。它们表现出行为改变、神经炎症、神经元丢失以及脑花生四烯酸（AA）酶增加。阿司匹林（乙酰水杨酸，ASA）通过环氧合酶（COX）-1和COX-2抑制AA氧化。
假说
慢性低剂量ASA将下调HIV-1转基因大鼠的脑AA代谢。
方法
给9个月大的HIV-1转基因和野生型大鼠在饮用水中给予42天10mg/kg/天的ASA或不给予任何处理；使用酶联免疫吸附测定法（ELISA）对微波处理的脑提取物进行类花生酸测量。
结果
HIV-1转基因大鼠的脑15-表-脂氧素A4和8-异前列腺素浓度显著高于野生型大鼠；这些差异被ASA阻止。ASA降低了HIV-1转基因大鼠而非野生型大鼠的前列腺素E2和白三烯B4浓度。血栓素B2、15-羟基二十碳四烯酸（15-HETE）、脂氧素A4和消退素D1浓度不受基因型或处理的影响。
结论
慢性低剂量ASA降低了HAND大鼠模型中神经炎症和氧化应激的AA代谢物标志物。
Zotero 插件