氧化应激和癫痫发作后细胞凋亡在重复癫痫后果中扮演着关键角色。有关α-蒎烯（APN）在某些神经退行性疾病实验模型中的益处已有报道。但是，它在由卡宾酸（KA）诱导的颞叶癫痫（TLE）大鼠模型中的神经保护功效还未被探索。我们旨在探究APN预处理在KA诱导的TLE大鼠模型中的可能抗抽搐效应及其潜在分子机制。使用KA经脑室内注射诱导雄性Wistar大鼠产生TLE。在诱导TLE前2周，以50mg/kg/d的剂量在腹腔内注射APN。在TLE诱导后的第一天，使用Racine评分记录和评价癫痫的行为表现。此外，还评估了海马的氧化应激指标，B细胞淋巴瘤2（Bcl2），Bcl2相关X蛋白（BAX）和c-Jun N末端激酶（JNK）蛋白水平。在TLE诱导后的第5天，使用Nissl染色对海马进行组织病理学评估。结果表明，APN预处理缓解了癫痫发作，减轻了氧化应激的指标，通过降低BAX和提高BCL2蛋白水平在海马中阻断了线粒体凋亡途径，至少部分地通过抑制JNK活性来降低了神经元死亡。这些发现揭示了APN预处理通过阻断氧化应激和神经损伤因素减轻了KA诱导的癫痫发作。可以得出结论，APN有潜在强大的抗癫痫药物的潜力，但需要进一步研究。 © 2023. 作者，独家许可Springer Science+Business Media，LLC（Springer Nature的一部分）。

Oxidative stress and apoptosis following seizures play pivotal roles in the consequences of repeated seizures. Beneficial effects of alpha-pinene (APN) have been reported in some experimental models of neurodegenerative diseases. However, its neuroprotective efficacy in a rat model of temporal lobe epilepsy (TLE) induced by kainic acid (KA) has remained unexplored. We aimed to explore the possible antiseizure effects of APN pretreatment and underlying molecular mechanisms in a rat model of TLE induced by KA. TLE was induced in male Wistar rats by intracerebroventricular injection of KA. APN at a dose of 50 mg/kg/day was intraperitoneally injected for 2 weeks before induction of TLE. One day after the induction of TLE, behavioral expressions of seizure were recorded and scored using Racine's scale. Furthermore, the hippocampal levels of oxidative stress markers, B-cell lymphoma 2 (Bcl2), BCL2-associated X protein (BAX), and c-Jun N-terminal kinase (JNK) protein levels were also assessed. Histopathological assessment in the hippocampus was performed with Nissl staining 5 days following induction of TLE. The results revealed that APN pretreatment alleviated epileptic seizures, diminished oxidative stress indicators, blocked the mitochondrial apoptotic pathway via decreasing BAX and raising BCL2 protein levels in the hippocampus at least partly through inhibiting JNK activity, and decreased neuronal death in the CA3 and hilus regions. These findings reveal that APN pretreatment mitigates KA-induced seizures by blocking oxidative stress and neuronal damage factors. It can be concluded that APN has a potent potential to be considered an antiseizure medication, but it needs further investigation.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.