Protective effect of naringin against ischemic reperfusion cerebral injury: Possible neurobehavioral, biochemical and cellular alterations in rat brain
Protective effect of naringin against ischemic reperfusion cerebral injury: Possible neurobehavioral, biochemical and cellular alterations in rat brain
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DOI：
10.1016/j.ejphar.2009.06.056
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发表时间：
2009-08-15
影响因子：
5
通讯作者：
Kumar, Anil
中科院分区：
文献类型：
--
作者：
Gaur, Vaibhav;Aggarwal, Aditi;Kumar, Anil
本研究旨在探讨柚皮苷对脑缺血再灌注所致的神经行为学改变、氧化损伤以及皮层、纹状体、海马区细胞和组织病理学改变的可能作用。雄性Wistar大鼠（200-220 g）双侧颈总动脉阻断30 min，再灌注24 h，诱导再灌注（I/R）脑损伤。柚苷（50、100 mg/kg，i. p.）在动物经受缺血再灌注损伤之前连续施用7天。随后评估了各种行为测试[自发活动、神经评分（斜梁测试）、转移潜伏期、对侧推的抵抗]和生化参数（脂质过氧化、亚硝酸盐水平、还原型谷胱甘肽、超氧化物歧化酶和过氧化氢酶活性）、大脑皮层、纹状体、海马中的线粒体酶功能障碍（复合物I、II、III和IV）以及组织病理学改变。与对照缺血再灌注相比，7天的柚皮苷（50和100 mg/kg）治疗显著改善了神经行为改变（改善了自发活动、斜梁行走和降低了对侧推的阻力、转移潜伏期）。柚苷（50 mg/kg和100 mg/kg）治疗显着减弱氧化损伤，如减少脂质过氧化反应，亚硝酸盐浓度，恢复还原型谷胱甘肽和过氧化氢酶活性和线粒体酶活性在皮层，纹状体，小脑相比，对照（缺血再灌注）动物。此外，柚苷治疗显着逆转皮质，纹状体，海马区的组织病理学改变相比，对照组（缺血再灌注）。目前的研究表明，柚皮苷对缺血再灌注诱导的大鼠行为学改变的保护作用及其治疗潜力。(C)2009 Elsevier B. V.保留所有权利。
The present study was conducted with an aim to explore the possible role of naringin against ischemia reperfusion induced-neurobehavioral alterations, oxidative damage, cellular and histo pathological alterations in cortex, striatum, hippocampus areas of brain. Male Wistar rats (200-220 g) were subjected to bilateral carotid artery occlusion for 30 min followed by reperfusion for 24 h to induce reperfusion (I/R) cerebral injury. Naringin (50, 100 mg/kg, i.p.) was administered for 7 days continuously before animals were subjected to ischemia reperfusion injury. Various behavioral tests [locomotor activity, neurological score (inclined beam test), transfer latency, resistance to lateral push] and biochemical parameters (lipid peroxidation, nitrite level, reduced glutathione, superoxide dismutase and catalase activity), mitochondrial enzyme dysfunctions (Complex I, II, III and IV) in cortex, striatum, hippocampus of brain and histopathological alterations were assessed subsequently. Seven days naringin (50 and 100 mg/kg) treatment significantly improved neurobehavioral alterations (improved locomotor activity, inclined beam walking and reduced resistance to lateral push, transfer latency) as compared to control ischemia reperfusion. Naringin (50 mg/kg and 100 mg/kg) treatment significantly attenuated oxidative damage as indicated by reduced lipid peroxidation, nitrite concentration, restored reduced glutathione and catalase activity and mitochondrial enzyme activities in cortex, striatum, cerebellum as compared to control (ischemia reperfusion) animals. In addition, naringin treatment significantly reversed histopathological alterations in cortex, striatum, hippocampus areas as compared to control (ischemia reperfusion). Present study suggests the protective effect of naringin and its therapeutic potential against ischemia reperfusion induced and related behavioral alterations in rats. (C) 2009 Elsevier B.V. All rights reserved.