Laboratorio de Investigaciones Antitrombóticas e Isquemia Tisular (LIAIT), Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain.
Neurosci Lett. 2010 Mar 3;471(2):89-93. doi: 10.1016/j.neulet.2010.01.017. Epub 2010 Jan 15.
Aspirin is the most widely used drug for the secondary prevention of ischemic stroke in patients suffering from diabetes mellitus. Moreover virgin olive oil (VOO) administration exerts a neuroprotective effect in healthy rat brain slices. The aim of the present study was to determine the possible influence of VOO administration to streptozotocin-diabetic rats (DR) on the neuroprotective effect of aspirin in rat brain. DR were treated during 3 months with saline, aspirin (2mg/kg/day p.o.), VOO (0.5 mL/kg/day p.o.) or its association; a control normoglycemic group was treated with saline. Brain slices were subjected to oxygen-glucose deprivation before a reoxygenation period. All the treatments significantly reduced lactate dehydrogenase LDH efflux after reoxygenation (-54.1% for aspirin, -51.3% for VOO and -72.9% for aspirin plus VOO). Lipid peroxides in brain slices were also reduced after the treatment with aspirin (-17.90%), VOO (-37.3%) and aspirin plus VOO (-49.2%). Production of nitric oxide after reoxygenation was inhibited by all the treatments (-46.5% for ASA, -48.2% for VOO and -75.8% for ASA plus VOO). The activity of the inducible isoform (iNOS) was inhibited by the three types of treatment (-31.8% for ASA, -29.1% for VOO and -56.0% for ASA plus VOO). The main conclusion of our study is that daily oral administration of VOO to diabetic rats may be a natural way to increase the neuroprotective effect of aspirin in diabetic animals.
阿司匹林是糖尿病患者缺血性中风二级预防中最常用的药物。此外,初榨橄榄油(VOO)在健康大鼠脑片中发挥神经保护作用。本研究旨在确定 VOO 给药对链脲佐菌素糖尿病大鼠(DR)对阿司匹林在大鼠脑中的神经保护作用的可能影响。DR 在 3 个月内用生理盐水、阿司匹林(2mg/kg/天 po)、VOO(0.5 mL/kg/天 po)或其组合治疗;对照组用生理盐水治疗。在再氧合期之前,脑片经历缺氧-葡萄糖剥夺。所有治疗均显著减少再氧合后乳酸脱氢酶 LDH 漏出(阿司匹林为-54.1%,VOO 为-51.3%,阿司匹林加 VOO 为-72.9%)。阿司匹林(-17.90%)、VOO(-37.3%)和阿司匹林加 VOO(-49.2%)治疗后脑片中的脂质过氧化物也减少。再氧合后一氧化氮的产生被所有治疗抑制(阿司匹林为-46.5%,VOO 为-48.2%,阿司匹林加 VOO 为-75.8%)。三种治疗方法均抑制诱导型同工酶(iNOS)的活性(阿司匹林为-31.8%,VOO 为-29.1%,阿司匹林加 VOO 为-56.0%)。我们研究的主要结论是,糖尿病大鼠每天口服 VOO 可能是增加糖尿病动物中阿司匹林神经保护作用的一种自然方式。