颞叶癫痫(TLE)的发展和进展受炎症的严重影响,胶质细胞的过度激活,和神经元细胞死亡。本研究旨在探讨α-pine烯(APN)治疗对促炎和抗炎细胞因子水平的影响,星形胶质增生,焦亡,海人酸(KA)诱导的TLE大鼠模型中海马中的自噬标记物。使用雄性Wistar大鼠,侧脑室注射KA诱导TLE。APN(50mg/kg)腹腔给药19天,包括KA给药前两周和给药后五天。从麻醉和KA注射完全恢复后,对癫痫发作相关行为表达进行评估.在第19天,海马IL-1β水平,TNF-α,前颗粒蛋白,IL-10,ERK1/2,磷酸化ERK1/2,NF-κB,GFAP,S100-B,检查了NLRP1,NLRP3,caspase-1和becline-1。结果显示,用APN治疗显著降低了IL-1β的升高水平,TNF-α,前颗粒蛋白,ERK1/2和NF-κB,并逆转了抗炎细胞因子水平的降低,IL-10,在由KA引起的海马中。此外,APN的施用显着降低了星形胶质细胞增生的水平,焦亡,和海马中的自噬标记被KA升高。可以得出结论,APN治疗19天可以通过抑制ERK1/2和NF-κB信号通路来减轻神经炎症,并防止星形胶质细胞增多。焦亡,TLE大鼠模型海马中的自噬标记物。
The development and progression of temporal lobe epilepsy (TLE) are heavily influenced by inflammation, excessive activation of glial cells, and neuronal cell death. This study aimed to investigate the effects of treatment with alpha-pinene (APN) on pro-and anti-inflammatory cytokine levels, astrogliosis, pyroptosis, and autophagy markers in the hippocampus in a rat model of TLE induced by kainic acid (KA). Male Wistar rats were employed, and TLE was induced by intracerebroventricular injection of KA. APN (50 mg/kg) was intraperitoneally administered for 19 days, including two weeks before and five days after the administration of KA. After full recovery from anesthesia and KA injection, the seizure-related behavioral expressions were evaluated. On day 19, the hippocampal levels of IL-1β, TNF-α, progranulin, IL-10, ERK1/2, phospho-ERK1/2, NF-κB, GFAP, S100-B, NLRP1, NLRP3, caspase-1, and becline-1 were examined. The results revealed that treatment with APN significantly diminished the heightened levels of IL-1β, TNF-α, progranulin, ERK1/2, and NF-κB and reversed the reduced levels of the anti-inflammatory cytokine, IL-10, in the hippocampus caused by KA. Furthermore, administration of APN significantly reduced the levels of astrogliosis, pyroptosis, and autophagy markers in the hippocampus that were elevated by KA. It can be concluded that treatment with APN for 19 days alleviated neuroinflammation by inhibiting ERK1/2 and NF-κB signaling pathways and prevented increases in astrogliosis, pyroptosis, and autophagy markers in the hippocampus in a rat model of TLE.