Çarçak Nihan, Mutlu Nursima, Erdeve Elif Tuğçe, Turan Talat Taygun, Sarıyıldız Özge, Ulusoy Canan, Şanlı Elif, Tüzün Erdem, Küçükali Cem İsmail, Brandolini Laura, Aramini Andrea, Allegretti Marcello, Onat Filiz, De Filippis Lidia
Department of Pharmacology, Faculty of Pharmacy, Istanbul University, 34116 Istanbul, Türkiye.
Department of Neuroscience, Institute of Health Sciences, Acibadem Mehmet Ali Aydinlar University, 34684 Istanbul, Türkiye.
Int J Mol Sci. 2025 Mar 21;26(7):2831. doi: 10.3390/ijms26072831.
Chemokine (CXC motif) ligand 8 (CXCL8) is a pro-inflammatory chemokine binding to CXC motif receptors 1/2 (CXCR1/2). Patients with temporal lobe epilepsy (TLE) exhibit increased serum CXCL8 levels. CXC motif ligand 1 (CXCL1), a murine ortholog of CXCL8, has been implicated in seizure generation and neuronal loss. This study evaluated the antiepileptogenic and antiseizure effects of reparixin in amygdaloid kindling rat model of TLE. Reparixin was administered during the kindling period for 14 days, and seizures were induced twice daily via electrical stimulation. To assess the antiseizure effects, reparixin was administered to fully kindled animals, and stimulations were performed 24 and 48 h later. Levetiracetam, a broad-spectrum antiseizure drug, was administered intraperitoneally (i.p.) as positive control 1 h before each stimulation. Reparixin delayed secondary seizure generalization during kindling. Reparixin reduced seizure severity and after-discharge duration in fully kindled animals at 24 h from treatment initiation. CXCR1/2 and protein kinase B pathway proteins exhibited no significant changes; reparixin reduced the phospho-extracellular signal-regulated kinase (pERK)/ERK ratio in the cortex and hippocampus. CXCL1 expression was significantly decreased in the cortex. Reparixin exhibited antiepileptogenic and partial antiseizure effects by modulating the CXCL1-CXCR1/2 axis and reducing ERK signaling. Already in clinical trials on respiratory diseases, reparixin could be repurposed for epilepsy therapy.
趋化因子(CXC基序)配体8(CXCL8)是一种与CXC基序受体1/2(CXCR1/2)结合的促炎趋化因子。颞叶癫痫(TLE)患者的血清CXCL8水平升高。CXCL8的小鼠同源物趋化因子(CXC基序)配体1(CXCL1)与癫痫发作的产生和神经元丢失有关。本研究评估了瑞帕霉素在TLE杏仁核点燃大鼠模型中的抗癫痫发生和抗癫痫作用。在点燃期给予瑞帕霉素14天,每天通过电刺激诱导癫痫发作两次。为了评估抗癫痫作用,将瑞帕霉素给予完全点燃的动物,并在24和48小时后进行刺激。左乙拉西坦是一种广谱抗癫痫药物,在每次刺激前1小时腹腔注射(i.p.)作为阳性对照。瑞帕霉素在点燃过程中延迟了继发性癫痫的泛化。从治疗开始24小时后,瑞帕霉素降低了完全点燃动物的癫痫严重程度和放电后持续时间。CXCR1/2和蛋白激酶B途径蛋白无显著变化;瑞帕霉素降低了皮质和海马中磷酸化细胞外信号调节激酶(pERK)/ERK的比值。皮质中CXCL1的表达显著降低。瑞帕霉素通过调节CXCL1-CXCR1/2轴并减少ERK信号传导,表现出抗癫痫发生和部分抗癫痫作用。在呼吸系统疾病的临床试验中,瑞帕霉素已可重新用于癫痫治疗。