Department of Medical Elementology and Toxicology (Fund for the Improvement of Science and Technology-DST and Special Assistance Programme-UGC Sponsored), Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, India.
Mol Cell Biochem. 2012 Aug;367(1-2):215-25. doi: 10.1007/s11010-012-1335-6. Epub 2012 May 22.
Stroke is a life-threatening disease with major cause of mortality and morbidity worldwide. The neuronal damage following cerebral ischemia is a serious risk to stroke patients. Oxidative stress and apoptotic damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The objective of this study was to test the hypothesis that administration of edaravone (Edv) maintains antioxidant status in brain, improves the cholinergic dysfunction and suppresses the progression of apoptosis response in rat. To test this hypothesis, male Wistar rats were subjected to middle cerebral artery occlusion (MCAO) of 2 h followed by reperfusion for 22 h. Edv was administered (10 mg/kg bwt) intraperitoneally 30 min before the onset of ischemia and 1 h after reperfusion. After reperfusion, rats were tested for neurobehavioral activities and were sacrificed for the infarct volume, estimation of oxidative damage markers. Edv treatment significantly reduced ischemic lesion volume, improved neurological deficits, contended oxidative loads, and suppressed apoptotic damage. In conclusion, treatment with Edv ameliorated the neurological and histological outcomes with elevated endogenous anti-oxidants status as well as reduced induction of apoptotic responses in MCA occluded rat. We theorized that Edv is among the pharmacological agents that reduce free radicals and its associated cholinergic dysfunction and apoptotic damage and have been found to limit the extent of brain damage following stroke.
中风是一种危及生命的疾病，是全球主要的死亡和发病原因。脑缺血后的神经元损伤是中风患者的严重风险。氧化应激和细胞凋亡损伤在脑缺血发病机制中起重要作用，可能是治疗的靶点。本研究旨在检验以下假设：依达拉奉（Edv）可维持大脑中的抗氧化状态，改善胆碱能功能障碍，并抑制大鼠细胞凋亡反应的进展。为了验证这一假设，雄性 Wistar 大鼠接受 2 小时大脑中动脉闭塞（MCAO），然后再灌注 22 小时。Edv 在缺血开始前 30 分钟和再灌注后 1 小时通过腹腔内给药（10mg/kg bwt）。再灌注后，大鼠进行神经行为活动测试，然后处死以测量梗死体积、估计氧化损伤标志物。Edv 治疗显著降低了缺血性损伤体积，改善了神经功能缺损，控制了氧化应激，并抑制了细胞凋亡损伤。总之，Edv 治疗改善了 MCA 闭塞大鼠的神经和组织学结局，提高了内源性抗氧化状态，减少了细胞凋亡反应的诱导。我们推测，Edv 是减少自由基及其相关胆碱能功能障碍和细胞凋亡损伤的药物之一，并已发现其可限制中风后脑损伤的程度。
