Student Research Committee, 48407Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Razi Drug Research Center, 440827Iran University of Medical Sciences, Tehran, Iran.
Hum Exp Toxicol. 2022 Jan-Dec;41:9603271221093989. doi: 10.1177/09603271221093989.
Epileptic seizures are associated with the release of potentially neurotoxic amount of glutamate, which results in the over-production of free radicals and inflammatory factors, and induction of neuronal cell death. Current study evaluated the effect of tannic acid (TA) on Kainic acid (KA)-induced seizures in mice.
Mice were divided into the six groups. Group I was administrated with normal saline (NS; 1 mL/kg, intraperitoneally (i.p.)), Group II was injected with KA (15 mg/kg, i.p.), Groups III was treated with diazepam (DZ; 20 mg/kg, i.p.) and KA (15 mg/kg, i.p.), Groups IV-VI were treated with TA (25, 50 and 100 mg/kg, i.p.) and KA (15 mg/kg, i.p.). Animals received all treatments 30 min before injection of KA. After the injection of KA, mice were observed for seizure (latency, activity and duration) and mortality for 2 h. In the brain tissue, oxidative stress, apoptosis, and inflammatory markers were evaluated in addition to the determination of histological alterations in the CA1 molecular layer of hippocampus.
reatment with TA significantly increased latency could not significantly decrease mice mortality. treatment with TA significantly improved KA-induced pyramidal cell loss and change in the arrangement of CA1 molecular layer.
Tannic acid may be useful in the control of epileptic seizures through regulating oxidative stress, inflammation and apoptosis.
癫痫发作与潜在神经毒性的谷氨酸释放有关，导致自由基和炎症因子的过度产生，并诱导神经元细胞死亡。本研究评估了单宁酸（TA）对海人酸（KA）诱导的小鼠癫痫发作的影响。
将小鼠分为六组。第 I 组给予生理盐水（NS；1 mL/kg，腹腔注射（i.p.）），第 II 组注射 KA（15 mg/kg，i.p.），第 III 组用地西泮（DZ；20 mg/kg，i.p.）和 KA（15 mg/kg，i.p.）处理，第 IV-VI 组用 TA（25、50 和 100 mg/kg，i.p.）和 KA（15 mg/kg，i.p.）处理。所有治疗均在注射 KA 前 30 分钟进行。注射 KA 后，观察小鼠 2 小时的癫痫发作（潜伏期、活动和持续时间）和死亡率。此外，还评估了脑组织中的氧化应激、细胞凋亡和炎症标志物，并测定了海马 CA1 分子层的组织学改变。
TA 治疗可显著延长潜伏期，但不能显著降低小鼠死亡率。TA 治疗可显著改善 KA 诱导的锥体神经元丢失和 CA1 分子层排列改变。
单宁酸可能通过调节氧化应激、炎症和细胞凋亡，有助于控制癫痫发作。
