Objective: Amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) is an ionotropic transmembrane receptor for glutamate. AMPA receptor blockers have been reported to prevent neurological damage and enhance the post stroke recovery in rats. Decanoic acid, a medium-chain fatty acid, has been reported to exhibit non-competitive AMPA receptor antagonism. This study evaluated the effect of decanoic acid administered before and after ischemia reperfusion injury on neurological damage and post stroke recovery in rats. Methods: Middle cerebral artery occlusion (MCAo) was performed by using the intraluminal method to induce focal cerebral ischemia. Decanoic acid (120 mg/kg) was administered orally for 1 day (5-10 min post reperfusion) in one group and for 2 days (24 h pre and 5-10 min post reperfusion) in the other group. Effect on neurological damage and post stroke recovery was assessed by neurobehavioral parameters, MRI and TTC staining along with inflammatory, oxidative, apoptotic, and neuroprotective biomarkers. Results: Decanoic acid significantly reduced the MCAo induced neurological damage and infarct size. Decanoic acid treatment increased the motor coordination and grip strength. Furthermore, levels of inflammatory (TNFα, IL-1β and IL-6), oxidative stress (MDA), apoptotic (TUNEL positive cells) and neurological injury (GFAP) biomarkers were reduced after decanoic acid treatment. Anti-inflammatory cytokine (IL-10) and neuroprotective markers (NT-3, BDNF and TrkB) were found to be significantly increased with decanoic acid treatment. Conclusion: This study showed protective effects of decanoic acid against ischemia reperfusion injury in rats. Anti-inflammatory, antioxidant, neuroprotective, and anti-apoptotic properties may be responsible for the beneficial effects of decanoic acid observed in the study.

目的：氨基-3-羟基-5-甲基-4-异恶唑丙酸酯 (AMPA) 是谷氨酸的离子型跨膜受体。据报道，AMPA 受体阻滞剂可预防神经损伤并增强大鼠中风后的恢复。据报道，癸酸是一种中链脂肪酸，具有非竞争性 AMPA 受体拮抗作用。本研究评估了在大鼠缺血再灌注损伤前后施用癸酸对神经损伤和中风后恢复的影响。方法：大脑中动脉闭塞（MCAo）是通过使用腔内方法来诱导局灶性脑缺血来进行的。一组口服癸酸 (120 mg/kg) 1 天（再灌注后 5-10 分钟），另一组口服 2 天（再灌注前 24 小时和再灌注后 5-10 分钟）。通过神经行为参数、MRI 和 TTC 染色以及炎症、氧化、细胞凋亡和神经保护生物标志物评估对神经损伤和中风后恢复的影响。结果：癸酸显着降低了 MCAo 诱导的神经损伤和梗塞面积。癸酸处理增加了运动协调性和握力。此外，在癸酸处理后，炎症（TNFα、IL-1β 和 IL-6）、氧化应激（MDA）、凋亡（TUNEL 阳性细胞）和神经损伤（GFAP）生物标志物的水平降低。抗炎细胞因子 (IL-10) 和神经保护标志物（NT-3、BDNF 和 TrkB）被发现随着癸酸处理而显着增加。结论：本研究表明癸酸对大鼠缺血再灌注损伤具有保护作用。抗炎、抗氧化、神经保护和抗细胞凋亡特性可能是研究中观察到的癸酸有益作用的原因。