Department of Anatomy, Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, 501 Jinjudaero, Jinju, 52828, South Korea.
Neurochem Res. 2018 Aug;43(8):1608-1623. doi: 10.1007/s11064-018-2576-x. Epub 2018 Jun 20.
Cerebral ischemia is a major cause of death and neurological disability. It also leads to severe brain tissue damage by excessive generation of oxidative stress. Quercetin is a bioflavonoid substance that acts an antioxidant agent and exerts a neuroprotective effect against cerebral ischemia. The aim of this study was to detect specific proteins that are differentially expressed in response to quercetin treatment in focal cerebral ischemia. Adult male rats were intraperitoneally injected with vehicle or quercetin (10 mg/kg) 30 min prior to right middle cerebral artery occlusion (MCAO). Brain tissues were collected 24 h after MCAO surgery and right cerebral cortices proteins were identified by two-dimensional gel electrophoresis and mass spectrometry. MCAO leads to neurological behavior disorders, infarction, and histopathological change. However, quercetin treatment alleviated MCAO-induced neuronal deficits and damages. We identified specific proteins differentially expressed between vehicle- and quercetin-treated animals. Among these detected proteins, isocitrate dehydrogenase [NAD], adenosylhomocysteinase, pyruvate kinase, and ubiquitin carboxy terminal hydrolase L1 were decreased in vehicle-treated animals, while quercetin administration alleviated the MCAO-induced decreases in these proteins. However, 60 kDa heat shock protein and collapsin response mediator protein 2 were increased in the vehicle-treated animals, and quercetin treatment attenuated increases in these proteins. The expression changes in these proteins were confirmed by Western blot and reverse transcription-PCR analyses. These proteins are associated with cellular differentiation, metabolism, and oxidative stress related proteins. These results suggest that quercetin reduces ischemic injury by modulating the expression of various proteins in focal cerebral ischemia.
脑缺血是死亡和神经功能障碍的主要原因。它还通过过度产生氧化应激导致严重的脑组织损伤。槲皮素是一种生物类黄酮物质，作为抗氧化剂，对脑缺血发挥神经保护作用。本研究旨在检测在局灶性脑缺血中，槲皮素处理后差异表达的特定蛋白质。成年雄性大鼠在右侧大脑中动脉闭塞（MCAO）前 30 分钟通过腹腔注射给予载体或槲皮素（10mg/kg）。MCAO 手术后 24 小时收集脑组织，并通过二维凝胶电泳和质谱法鉴定右大脑皮质蛋白质。MCAO 导致神经行为障碍、梗塞和组织病理学改变。然而，槲皮素治疗减轻了 MCAO 诱导的神经元缺陷和损伤。我们鉴定了载体和槲皮素处理动物之间差异表达的特定蛋白质。在这些检测到的蛋白质中，异柠檬酸脱氢酶[NAD]、腺苷同型半胱氨酸酶、丙酮酸激酶和泛素羧基末端水解酶 L1 在载体处理的动物中减少，而槲皮素给药减轻了 MCAO 诱导的这些蛋白质减少。然而，60kDa 热休克蛋白和崩溃反应调节剂蛋白 2 在载体处理的动物中增加，槲皮素治疗减轻了这些蛋白质的增加。通过 Western blot 和逆转录-PCR 分析证实了这些蛋白质的表达变化。这些蛋白质与细胞分化、代谢和与氧化应激相关的蛋白质有关。这些结果表明，槲皮素通过调节局灶性脑缺血中各种蛋白质的表达来减轻缺血性损伤。
