首页> 外文期刊>European Journal of Pharmacology: An International Journal >Protective effect of naringin against ischemic reperfusion cerebral injury: possible neurobehavioral, biochemical and cellular alterations in rat brain.
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Protective effect of naringin against ischemic reperfusion cerebral injury: possible neurobehavioral, biochemical and cellular alterations in rat brain.

机译:柚皮苷对缺血性再灌注性脑损伤的保护作用:大鼠脑中可能的神经行为,生化和细胞改变。

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摘要

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 histopathological 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.
机译:进行本研究的目的是探讨柚皮苷对缺血再灌注诱导的大脑皮层,纹状体,海马区的神经再灌注改变,氧化损伤,细胞和组织病理学改变的可能作用。对雄性Wistar大鼠(200-220 g)进行双侧颈动脉闭塞30分钟,然后再灌注24小时,以诱发再灌注(I / R)脑损伤。在使动物遭受缺血再灌注损伤之前,连续7天服用柚皮苷(50,100mg / kg,腹膜内)。各种行为测试(运动能力,神经学评分(斜射束测试),转移潜伏期,对侧推的抵抗力)和生化参数(脂质过氧化,亚硝酸盐水平,谷胱甘肽降低,超氧化物歧化酶和过氧化氢酶活性),线粒体酶功能异常(复合体I,随后评估大脑皮层,纹状体,海马中的II,III和IV和组织病理学改变。与对照缺血再灌注相比,柚皮素(50和100 mg / kg)的七天治疗显着改善了神经行为改变(改善了运动能力,倾斜束行走并降低了对侧推的抵抗力,转移潜伏期)。柚皮苷(50 mg / kg和100 mg / kg)治疗显着减轻了氧化损伤,表现为脂质过氧化减少,亚硝酸盐浓度降低,皮层,纹状体,小脑中还原型谷胱甘肽和过氧化氢酶活性以及线粒体酶活性降低(与缺血再灌注相比) ) 动物。此外,与对照相比,柚皮苷治疗显着逆转了皮质,纹状体,海马区的组织病理学改变(缺血再灌注)。目前的研究表明柚皮苷的保护作用及其对大鼠缺血再灌注及相关行为改变的治疗潜力。

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