Human & Experimental Toxicology · 2020 · 15 citations · 40 references
MedicineNeurosciencePharmacologyMemoryNeurochemistryNeuropharmacologyAddictionAddiction NeurobiologyBiomarkers Of NeurotoxicityNeural Basis Of MemoryNeuroprotectionOxidative Stress In NeurotoxicityGlutathione Peroxidase ActivityHippocampal Memory FunctionHippocampal Neuron LossHippocampal ToxicityMalondialdehyde FormationNeurotoxic Plant CompoundsOxidative Stress InjuryPro-apoptotic Protein Loss
AIM OF STUDY: This investigation evaluated the capacity of epigallocatechin-3-gallate (EGCG) as the main polyphenolic compound in the green tea extract against memory impairment and neurotoxicity in morphine-treated rats. METHODS: To measure the EGCG effect (5 and 50 mg/kg, i.p., co-treated with morphine) on spatial learning and memory of morphine-administrated male Wistar rats (45 mg/kg, s.c., 4 weeks), the Morris water maze test was used. Some apoptotic protein levels (Bax, Bcl-2, and cleaved caspase 3) were evaluated in the hippocampus tissue by the Western blot test. Also, oxidative stress status (malondialdehyde level, glutathione peroxidase, and superoxide dismutase activity) was measured in hippocampus tissue. RESULTS: The data presented that EGCG treatment (50 mg/kg) inhibited the morphine-induced memory deficits in rats. Also, EGCG administration reduced the apoptosis and oxidative stress in the hippocampus of morphine-treated rats. CONCLUSIONS: Our data indicate that EGCG can improve memory in morphine-treated rats. Molecular mechanisms underlying the detected effects could be related to the prevention of apoptosis and oxidative stress in the hippocampus of morphine-treated rats.
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