Ischemic stroke is a leading cause of human mortality. Cerebral ischemia–reperfusion injury (CI/RI) is a primary cause of stroke. Ischemia–reperfusion (I/R) resulting in oxidative stress and inflammatory events may lead to severe neuronal impairments. Thus, anti‐oxidative and anti‐inflammatory mediators that can alleviate post‐I/R neuronal injuries are required for the treatment of CI/RI. An alkaloid, voacangine (VCG) is a recognized antioxidant, anti‐inflammatory, and anticancer agent. Hence, the current study intended to explore the neuroprotective potential and the principal mechanisms of VCG in CI/RI. The experimental rats were divided into four sets: control, I/R‐induced, I/R + VCG (2.5 mg/kg), I/R + VCG (5 mg/kg). CI/RI was induced by implanting a thread into the middle cerebral artery occlusion (MCAO) model. Brain damages were assessed on the basis of brain edema, brain infarct volume, neurological deficit score, histopathology, oxidative stress, and neuroinflammation. Results revealed that VCG inhibited the triggering of NLRP3 inflammasome, pro‐inflammatory cytokines, lipid peroxidation, but enhanced the antioxidant status in MCAO rats. Furthermore, VCG treatment averted brain damage by I/R, neuroinflammation, and oxidative stress by suppressing NF‐κBp65/MAPK pathways. The results of the study provide pertinent insights pertaining to the role of VCG as a potential neuroprotective agent against ischemic stroke.

中文翻译：

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Voacangine 通过逆转 NF-κBp65/MAPK 信号通路减轻大脑中动脉闭塞引起的脑缺血/再灌注损伤中的氧化应激和神经炎症

缺血性中风是人类死亡的主要原因。脑缺血再灌注损伤（CI/RI）是中风的主要原因。缺血再灌注（I/R）导致氧化应激和炎症事件，可能导致严重的神经元损伤。因此，CI/RI 的治疗需要能够减轻 I/R 后神经元损伤的抗氧化和抗炎介质。 voacangine (VCG) 是一种生物碱，是一种公认​​的抗氧化剂、抗炎剂和抗癌剂。因此，本研究旨在探讨 VCG 在 CI/RI 中的神经保护潜力和主要机制。实验大鼠分为四组：对照组、I/R诱导组、I/R + VCG (2.5 mg/kg)、I/R + VCG (5 mg/kg)。 CI/RI是通过将线植入大脑中动脉闭塞（MCAO）模型来诱导的。根据脑水肿、脑梗塞体积、神经功能缺损评分、组织病理学、氧化应激和神经炎症评估脑损伤。结果显示，VCG 抑制 NLRP3 炎症小体、促炎细胞因子、脂质过氧化的触发，但增强 MCAO 大鼠的抗氧化状态。此外，VCG 治疗通过抑制 NF-κBp65/MAPK 通路，避免了 I/R、神经炎症和氧化应激引起的脑损伤。该研究的结果提供了有关 VCG 作为抗缺血性中风的潜在神经保护剂的作用的相关见解。