Gaur Vaibhav, Aggarwal Aditi, Kumar Anil
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.
Indian J Exp Biol. 2011 Aug;49(8):609-18.
Stroke is the third leading cause of death and disability around the globe. The aim of the present investigation was to evaluate the protective effect of hesperidin and its nitric oxide mechanism against cerebral ischemia reperfusion injury. Bilateral common carotid artery occlusion for 30 min followed by 24 h reperfusion was given to induce ischemia in rats. Animals were pretreated with hesperidin (50 and 100 mg/kg, po) for 7 days. Various behavioural tests, oxidative stress parameters, endogenous antioxidant system, antioxidant enzyme activity and mitochondrial enzyme complex (I, II, III and IV) dysfunctions in cortex and striatum were assessed subsequently. Hesperidin (50 and 100 mg/kg) significantly improved neurobehavioral alterations (neurological score, locomotor activity, resistance to lateral push and hanging wire latency), attenuated oxidative damage, restored antioxidant and mitochondrial complex enzyme activities in cortex and in striatum regions of the brain as compared to their respective controls. L-arginine (100 mg/kg) or L-NAME (10 mg/kg) pretreatment with lower dose of hesperidin (50 mg/kg) significantly reversed or potentiated its protective effect, respectively which was significant as compared to hesperidin (50 mg/kg). The results highlight the involvement of nitric oxide mechanism in the protective effect of hesperidin against ischemia reperfusion injury induced alterations.
中风是全球第三大致死和致残原因。本研究的目的是评估橙皮苷的保护作用及其一氧化氮机制对脑缺血再灌注损伤的影响。通过对大鼠双侧颈总动脉进行30分钟的闭塞，然后再灌注24小时来诱导缺血。动物用橙皮苷（50和100毫克/千克，口服）预处理7天。随后评估了各种行为测试、氧化应激参数、内源性抗氧化系统、抗氧化酶活性以及大脑皮质和纹状体中的线粒体酶复合物（I、II、III和IV）功能障碍。与各自的对照组相比，橙皮苷（50和100毫克/千克）显著改善了神经行为改变（神经评分、运动活动、对侧向推挤的抵抗力和悬线潜伏期），减轻了氧化损伤，恢复了大脑皮质和纹状体区域的抗氧化和线粒体复合酶活性。用L-精氨酸（100毫克/千克）或L-硝基精氨酸甲酯（10毫克/千克）预处理低剂量的橙皮苷（50毫克/千克），分别显著逆转或增强了其保护作用，与橙皮苷（50毫克/千克）相比具有显著性。结果突出了一氧化氮机制在橙皮苷对缺血再灌注损伤诱导的改变的保护作用中的参与。
