Ischemic stroke is a medical condition that arises because of poor blood supply to the brain. Reperfusion being salvage to the brain further causes, exacerbation of tissue injury, known as reperfusion injury. Ischemic preconditioning (IPC) has been known to provide benefits against ischemia reperfusion (I/R) injury. Dopamine D2/D3 receptor mediated several pathways are also reported as mediators in the IPC mediated neuroprotection. This study investigates the possible involvement of D2/D3 receptor activation in IPC mediated neuroprotection in the I/R brain. Global cerebral ischemia/reperfusion (GCI/R) injury in swiss albino mice was induced by occluding the common carotid arteries for 17 min, followed by 24 h reperfusion. IPC was provided by giving 3 episodes of I/R prior to Ischemia (17 min). Morris water maze (MWM) was used to assess the spatial learning, memory and Rota rod, lateral push test as well as inclined beam test were conducted to assess the motor functions in animals. Cerebral oxidative markers (thiobarbituric acid reactive species-TBARS, reduced glutathione-GSH, superoxide dismutase-SOD, and catalase-CAT), inflammatory markers (IL-6, IL-10, TNF-α, and myeloperoxidase-MPO), acetylcholinesterase activity-AChE, infarct size (% weight and % volume), and histopathological changes were also assessed. Haloperidol (0.05 mg/kg, i.p) was used to antagonize the effects of D2/D3 receptor activation. I/R animals showed reduction in memory, motor function, increase in cerebral oxidative stress, inflammation, AChE activity, infarct size and histopathological changes. Episodes of IPC prior to ischemia, attenuated the deleterious effects of I/R injury. Administration of haloperidol abolished the protective effects of IPC. Hence, it may be concluded that IPC mediated neuroprotection may involves dopamine D2/D3 receptor activation in mice.

缺血性中风是一种由于大脑供血不足而引起的疾病。再灌注对大脑的抢救会进一步导致组织损伤的加剧，称为再灌注损伤。已知缺血预处理 (IPC) 可提供对抗缺血再灌注 (I/R) 损伤的益处。多巴胺 D2/D3 受体介导的几种途径也被报道为 IPC 介导的神经保护中的介质。本研究调查了 D2/D3 受体激活可能参与 I/R 大脑中 IPC 介导的神经保护。瑞士白化小鼠的全脑缺血/再灌注 (GCI/R) 损伤是通过阻塞颈总动脉 17 分钟，然后再灌注 24 小时来诱导的。IPC 通过在缺血前进行 3 次 I/R 发作（17 分钟）来提供。Morris水迷宫(MWM)用于评估动物的空间学习、记忆和旋转杆，进行侧推试验以及斜梁试验来评估动物的运动功能。脑氧化标志物（硫代巴比妥酸反应性物质-TBARS、还原型谷胱甘肽-GSH、超氧化物歧化酶-SOD 和过氧化氢酶-CAT）、炎症标志物（IL-6、IL-10、TNF-α 和髓过氧化物酶-MPO）、乙酰胆碱酯酶活性-AChE、梗塞大小（重量百分比和体积百分比）和组织病理学变化也被评估。氟哌啶醇 (0.05 mg/kg, ip) 用于拮抗 D2/D3 受体激活的影响。I/R 动物表现出记忆力下降、运动功能下降、脑氧化应激增加、炎症、乙酰胆碱酯酶活性、梗塞面积和组织病理学变化。缺血前 IPC 发作，减弱了 I/R 损伤的有害影响。氟哌啶醇的给药消除了 IPC 的保护作用。因此，可以得出结论，IPC 介导的神经保护可能涉及小鼠多巴胺 D2/D3 受体的激活。