Lupeol has been reported to exhibit anti-inflammatory and anti-tumor activities in many diseases, but its potential effects in cerebral ischemia injury have not been studied to date. In this work we present evidence for a beneficial effect of lupeol in a rat model of middle cerebral artery occlusion (MCAO) followed by reperfusion (MCAO/R) injury and provide some histological and biochemical evidence for its mechanism of action. A cerebral MCAO rat model was established by vascular occlusion for 2 h, followed by 24 h reperfusion period. The infarct volume, neurological deficits, and brain water content were compared with animals treated during reperfusion with different concentrations of lupeol. Macroscopic parameters, cell viability, pro-inflammatory factors generation, as well as oxidative stress parameters and associated apoptotic signaling cascades were evaluated. Treatment with lupeol significantly reduced the cerebral infarct volume and water content and recovered neuro behavioral functions in affected rats. Lupeol treatment down-regulated the expression of oxidative stress and inflammation factors. In addition, lupeol activated Nrf2, suppressed caspase-3 activity, reduced BAX/Bcl-2 ratio and inhibited phosphorylation of p38 MAPK. The data suggest that lupeol may exert protective effects against cerebral ischemia by suppressing oxidative stress and reduction of inflammation factors possible via activation of nuclear transcription factors and inhibition of cell death pathways.

中文翻译：

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Lupeol 对大鼠大脑中动脉诱导的脑缺血的有益影响涉及 Nrf2 和 P38 MAPK 调节。

据报道，羽扇豆醇在许多疾病中表现出抗炎和抗肿瘤活性，但迄今为止尚未研究其在脑缺血损伤中的潜在作用。在这项工作中，我们提供了羽扇豆醇在大脑中动脉闭塞 (MCAO) 后再灌注 (MCAO/R) 损伤的大鼠模型中的有益作用的证据，并为其作用机制提供了一些组织学和生化证据。血管闭塞2 h，再灌注24 h，建立脑MCAO大鼠模型。将梗塞体积、神经功能缺损和脑水含量与再灌注期间用不同浓度羽扇豆醇治疗的动物进行比较。宏观参数、细胞活力、促炎因子的产生、以及氧化应激参数和相关的凋亡信号级联反应进行了评估。羽扇豆醇治疗显着减少了脑梗塞体积和水含量，并恢复了受影响大鼠的神经行为功能。Lupeol 治疗下调氧化应激和炎症因子的表达。此外，羽扇豆醇激活 Nrf2，抑制 caspase-3 活性，降低 BAX/Bcl-2 比率并抑制 p38 MAPK 的磷酸化。数据表明羽扇豆醇可能通过激活核转录因子和抑制细胞死亡途径来抑制氧化应激和减少炎症因子，从而对脑缺血发挥保护作用。羽扇豆醇治疗显着减少了脑梗塞体积和水含量，并恢复了受影响大鼠的神经行为功能。Lupeol 治疗下调氧化应激和炎症因子的表达。此外，羽扇豆醇激活 Nrf2，抑制 caspase-3 活性，降低 BAX/Bcl-2 比率并抑制 p38 MAPK 的磷酸化。数据表明羽扇豆醇可能通过激活核转录因子和抑制细胞死亡途径来抑制氧化应激和减少炎症因子，从而对脑缺血发挥保护作用。羽扇豆醇治疗显着减少了脑梗塞体积和水含量，并恢复了受影响大鼠的神经行为功能。Lupeol 治疗下调氧化应激和炎症因子的表达。此外，羽扇豆醇激活 Nrf2，抑制 caspase-3 活性，降低 BAX/Bcl-2 比率并抑制 p38 MAPK 的磷酸化。数据表明羽扇豆醇可能通过激活核转录因子和抑制细胞死亡途径来抑制氧化应激和减少炎症因子，从而对脑缺血发挥保护作用。降低 BAX/Bcl-2 比率并抑制 p38 MAPK 的磷酸化。数据表明羽扇豆醇可能通过激活核转录因子和抑制细胞死亡途径来抑制氧化应激和减少炎症因子，从而对脑缺血发挥保护作用。降低 BAX/Bcl-2 比率并抑制 p38 MAPK 的磷酸化。数据表明羽扇豆醇可能通过激活核转录因子和抑制细胞死亡途径来抑制氧化应激和减少炎症因子，从而对脑缺血发挥保护作用。