EFFECTS OF AMENTOFLAVONE ON HIPPOCAMPAL NEURON DAMAGE AND OXIDATIVE STRESS IN DRUG-INDUCED EPILEPTIC RATS

Xiaoquan Li^{1, #}, Jia Liu^{2, #}, Jianhua Yang³, Zhaohui Lai^{3, *} 

¹Department of Neurology, Songgang People's Hospital of Bao'an District, Shenzhen, 518105, China - ²Department of Endocrinology, Ganzhou People's Hospital of Jiangxi Province, Ganzhou, 341001, China - ³Department of Neurology, Ganzhou People's Hospital of Jiangxi Province, Ganzhou, 341001, China

Objective: To analyze the effects of amentoflavone (AF) on neuronal damage and oxidative stress in epileptic rats induced by drugs. 

Methods: Fifteen disease-free SD rats were randomly divided into an AF intervention group, a model group, and a blank control group, with five rats in each group. The AF intervention group was given an intraperitoneal injection of 25 mg/kg AF for five consecutive days, while the model group and blank control group were given intraperitoneal injections of the same amount of normal saline. On the fifth day, the AF intervention group and the model group were intraperitoneally injected with lithium chloride 127 mg/kg. After 18 hours, 30 mg/kg pilocarpine was injected intraperitoneally to induce seizures. A Morris water maze test of rat behavioral responses, immunohistochemical methods, and the ELISA method was used to detect the positive expression and activity of NF-κB p65 and to compare oxidative stress indicators (MAD, SOD, GSH) of rats in each group. 

Results: The escape latency time of the model group was significantly longer than that of the blank control group (P<0.05), and the times to pass through the original platform were significantly less compared to the blank control group (P<0.05). The escape latency time of the AF intervention group was significantly shorter than that of the model group (P<0.05), and the times to pass through the original platform were significantly greater than those of the model group (P<0.05). Rat hippocampus NF-κB p65 positive cells showed different degrees of brown expression. The number of NF-κB p65 positive cells in the model group was significantly greater compared to the blank control group (P<0.05), and the number of NF-κB p65 positive cells in the AF intervention group was significantly less than that in the model group (P<0.05). The hippocampal NF-κB p65 activity concentration of the model group was significantly higher than that of the blank control group (P<0.05), and the hippocampal NF-κB activity concentration of the AF intervention group was significantly lower compared to the model group, a difference that was statistically significant (P<0.05). The MDA content was significantly higher in the model group compared to the blank control group, and the SOD and GSH content was significantly lower compared to the blank control group (P<0.05). Additionally, the MDA content of the AF intervention group was significantly lower than that of the model group, and the SOD and GSH content was significantly higher than that of the model group (P<0.05). 

Conclusion: Amentoflavone can significantly reduce hippocampal neuronal damage in epileptic rats, inhibit oxidative stress reaction, and play a neuroprotective role, which warrants further exploration for potential clinical application.