Cerebral ischemia is a major health threat to humankind around the world, and the reperfusion methods may provoke irreversible damages to brain tissues, causing impairment of neurological function. The goal of this study is to investigate the potential neurological protective effect of PJ34, a well-characterized poly (ADP-ribose) polymerase 1 (PARP-1) inhibitor, on cerebral ischemia–reperfusion (I/R)-induced injury of the rat model. The cerebral I/R rats were received (3, 6, or 12 mg/kg) injections of PJ34 or saline at 24 h, 6 h before middle cerebral artery occlusion (MCAO) and 1 h, 24 h, and 48 h after MCAO. All rats were subject to the neurological behavior tests by open field test and Morris water maze test. The expression of pro-inflammatory cytokines, Cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) in cerebral tissues was also determined. Our results demonstrated that the administration of PJ34 dose-dependently ameliorated cerebral I/R-induced injury and improved neurological performance of cerebral I/R rats. We also revealed that PJ34 treatment effectively reduced COX2, iNOS, and pro-inflammatory cytokine levels in the I/R-induced injury tissues. Our finding further supports that inhibition of PARP-1 activity is beneficial for reducing post-I/R-induced brain damage via targeting inflammatory response.

脑缺血是世界范围内对人类健康的主要威胁，再灌注方法可能对脑组织造成不可逆的损伤，导致神经功能受损。本研究的目的是研究 PJ34 对脑缺血再灌注 (I/R) 引起的脑缺血再灌注损伤的潜在神经保护作用。大鼠模型。大脑 I/R 大鼠在大脑中动脉闭塞 (MCAO) 前 24 小时、6 小时和 MCAO 后 1、24 和 48 小时接受（3、6 或 12 mg/kg）PJ34 或生理盐水注射. 所有大鼠均通过旷场试验和Morris水迷宫试验进行神经行为学试验。促炎细胞因子的表达，还测定了脑组织中的环氧合酶 2 (COX-2) 和诱导型一氧化氮合酶 (iNOS)。我们的研究结果表明，PJ34 的给药剂量依赖性地改善了脑 I/R 诱导的损伤并改善了脑 I/R 大鼠的神经功能。我们还发现，PJ34 治疗有效降低了 I/R 诱导的损伤组织中的 COX2、iNOS 和促炎细胞因子水平。我们的发现进一步支持 PARP-1 活性的抑制有利于通过靶向炎症反应减少 I/R 后诱导的脑损伤。和 I/R 诱导的损伤组织中的促炎细胞因子水平。我们的发现进一步支持 PARP-1 活性的抑制有利于通过靶向炎症反应减少 I/R 后诱导的脑损伤。和 I/R 诱导的损伤组织中的促炎细胞因子水平。我们的发现进一步支持 PARP-1 活性的抑制有利于通过靶向炎症反应减少 I/R 后诱导的脑损伤。