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辅酶Q(10)对大鼠脑实验性缺血生化及形态学变化的影响。

Effect of coenzyme Q(10) on biochemical and morphological changes in experimental ischemia in the rat brain.

作者信息

Ostrowski R P

机构信息

Laboratory of Clinical Neurochemistry, Department of Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

出版信息

Brain Res Bull. 2000 Nov 1;53(4):399-407. doi: 10.1016/s0361-9230(00)00406-8.

Abstract

The aim of the work was to evaluate an influence of CoQ(10) on lactate acidosis, adenosine-5'-triphosphate (ATP) concentrations, oxidized to reduced glutathione ratio and on superoxide dismutase activity in endothelin model of cerebral ischemia in the rat. Light microscopic studies in the central nervous system and morphometric analysis of pyramidal cells in the hippocampus were also performed. Endothelins (ET-1 or ET-3; 20 pmoles) were injected into the right lateral cerebral ventricle (intracerebroventricularly). CoQ(10) was given intraperitoneally (i.p.) just before the operation (i.p. 10 mgkg b. wt.). More severe changes of investigated biochemical parameters were observed in the animals treated with ET-1 in comparison with ET-3. Recovery was noted earlier in the group subjected to ET-3 and CoQ(10) administration, than in the animals subjected to ET-1 and CoQ(10) treatment. Histopathological observations showed sparse foci of a neuronal loss in the cerebral cortex and in the hippocampus only in the ET-1 model of ischemia. Additionally more numerous dark neurons were present in above brain structures following ET-1 administration comparing with ET-3 one. Morphometrical studies demonstrated that CoQ(10) diminished neuronal injury in the hippocampal CA1, CA2 and CA3 zones. Above data indicate on neuroprotective effect of CoQ(10) as a potent antioxidant and oxygen derived free radicals scavenger in the cerebral ischemia.

摘要

这项工作的目的是评估辅酶Q10对大鼠脑缺血内皮素模型中乳酸酸中毒、三磷酸腺苷(ATP)浓度、氧化型谷胱甘肽与还原型谷胱甘肽的比值以及超氧化物歧化酶活性的影响。还对中枢神经系统进行了光学显微镜研究,并对海马体中的锥体细胞进行了形态计量分析。将内皮素(ET-1或ET-3;20皮摩尔)注入右侧侧脑室(脑室内)。在手术前腹腔注射辅酶Q10(腹腔注射10毫克/千克体重)。与ET-3相比,接受ET-1治疗的动物中观察到所研究的生化参数有更严重的变化。在接受ET-3和辅酶Q10给药的组中,恢复比接受ET-1和辅酶Q10治疗的动物更早出现。组织病理学观察显示,仅在ET-1缺血模型中,大脑皮层和海马体中有稀疏的神经元丢失灶。此外,与ET-3给药后相比,ET-1给药后上述脑结构中出现了更多的暗神经元。形态计量学研究表明,辅酶Q10减少了海马体CA1、CA2和CA3区的神经元损伤。上述数据表明辅酶Q10作为一种有效的抗氧化剂和氧衍生自由基清除剂在脑缺血中具有神经保护作用。

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