Evaluation of the neuroprotective effect of taurine and green tea extract against oxidative stress induced by pilocarpine during status epilepticus

Autor: Neveen A. Noor, Haitham S. Mohammed, Yasser A. Khadrawy, Heba S. Aboul Ezz, Nasr M. Radwan
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Zdroj: Journal of Basic and Applied Zoology, Vol 72, Iss C, Pp 8-15 (2015)
Druh dokumentu: article
ISSN: 2090-9896
DOI: 10.1016/j.jobaz.2015.02.001
Popis: Status epilepticus (SE) has functional and structural consequences resulting in brain damage. The present study aims to investigate the role of taurine and green tea extract in the neuroprotection against oxidative stress and changes in acetylcholinesterase (AChE) and Na+,K+-ATPase activities during SE induced by pilocarpine in the hippocampus of adult male rats. Animals received an oral administration of either taurine (100 mg/kg) or green tea extract containing 100 mg/kg epigallocatechin gallate for 3 days before the induction of SE with pilocarpine (380 mg/kg, i.p.) and were sacrificed 1 h after pilocarpine injection. Data indicated that a state of oxidative stress has evolved during SE as evident from the significant increase in lipid peroxidation level and significant decrease in reduced glutathione (GSH) level. Significant decreases in AChE and Na+,K+-ATPase activities were also recorded. Pretreatment of rats with taurine exaggerated the increase in lipid peroxidation and failed to prevent the decrease in Na+,K+-ATPase activity resulting from pilocarpine. However, taurine pretreatment prevented the reduced activity of hippocampal AChE induced by pilocarpine during SE. Pretreatment of rats with green tea extract prevented the increase in lipid peroxidation occurring during SE. However, it failed to inhibit the decrease in Na+,K+-ATPase activity. In conclusion, taurine pretreatment failed to reduce the oxidative stress induced during SE. In contrast, pretreatment of rats with green tea extract ameliorated the oxidative stress induced by pilocarpine and this may assist in reducing the insults of hyperexcitability and excitotoxicity that occur during SE and thereby reduce neuronal damage.
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