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首页> 外文期刊>The FEBS journal >Modulation of the endocannabinoid system by focal brain ischemia in the rat is involved in neuroprotection afforded by 17 beta-estradiol
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Modulation of the endocannabinoid system by focal brain ischemia in the rat is involved in neuroprotection afforded by 17 beta-estradiol

机译：大鼠局灶性脑缺血对内源性大麻素系统的调节参与17β-雌二醇提供的神经保护作用

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Endogenous levels of the endocannabinoid anandamide, and the activities of the synthesizing and hydrolyzing enzymes, i.e. N-acylphosphatidylethanolamine-hydrolyzing phospholipase D and fatty acid amide hydrolase, respectively, were determined in the cortex and the striatum of rats subjected to transient middle cerebral artery occlusion. Anandamide content was markedly increased (similar to 3-fold over controls; P < 0.01) in the ischemic striatum after 2 h of middle cerebral artery occlusion, but not in the cortex, and this elevation was paralleled by increased activity of N-acylphosphatidylethanolamine-hydrolyzing phospholipase D (similar to 1.7-fold; P < 0.01), and reduced activity (similar to 0.6-fold; P < 0.01) and expression (similar to 0.7-fold; P < 0.05) of fatty acid amide hydrolase. These effects of middle cerebral artery occlusion were further potentiated by 1 h of reperfusion, whereas anandamide binding to type 1 cannabinoid and type 1 vanilloid receptors was not affected significantly by the ischemic insult. Additionally, the cannabinoid type 1 receptor antagonist SR141716, but not the receptor agonist R-(+)-WIN55,212-2, significantly reduced (33%; P < 0.05) cerebral infarct volume detected 22 h after the beginning of reperfusion. A neuroprotective intraperitoneal dose of 17 beta-estradiol (0.20 mg.kg(-1)) that reduced infarct size by 43% also minimized the effect of brain ischemia on the endocannabinoid system, in an estrogen receptor-dependent manner. In conclusion, we show that the endocannabinoid system is implicated in the pathophysiology of transient middle cerebral artery occlusion-induced brain damage, and that neuroprotection afforded by estrogen is coincident with a re-establishment of anandamide levels in the ischemic striatum through a mechanism that needs to be investigated further.
机译：在短暂性脑中动脉阻塞的大鼠的皮层和纹状体中，分别测定了内源性内源性大麻素大麻酚水平以及合成和水解酶（即N-酰基磷脂酰乙醇胺水解磷脂酶D和脂肪酸酰胺水解酶）的活性。 。大脑中部动脉闭塞2小时后，缺血性纹状体中Anandamide含量显着增加（比对照高3倍; P <0.01），但在皮质中却没有，而这种升高与N-酰基磷脂酰乙醇胺-水解磷脂酶D（约1.7倍; P <0.01），并降低脂肪酸酰胺水解酶的活性（约0.6倍; P <0.01）和表达（约0.7倍; P <0.05）。再灌注1 h进一步增强了大脑中动脉闭塞的这些作用，而缺血性损伤并未显着影响anandamide与1型大麻素和1型香草类受体的结合。此外，大麻素1型受体拮抗剂SR141716，但不是受体激动剂R-（+）-WIN55,212-2，在再灌注开始后22 h显着减少了（33％; P <0.05）脑梗死体积。腹膜内给予17β-雌二醇（0.20 mg.kg（-1））的神经保护性剂量可将梗塞面积减少43％，并以雌激素受体依赖性方式将脑缺血对内源性大麻素系统的影响降至最低。总之，我们表明，内源性大麻素系统与短暂性大脑中动脉闭塞引起的脑损伤的病理生理有关，并且雌激素提供的神经保护作用与缺血性纹状体中anandamide水平的重新建立是一致的，其机制需要有待进一步调查。

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