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1.
Hum Exp Toxicol ; 39(7): 994-1002, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32129083

RESUMO

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.


Assuntos
Catequina/análogos & derivados , Transtornos da Memória/tratamento farmacológico , Morfina/toxicidade , Fármacos Neuroprotetores/uso terapêutico , Síndromes Neurotóxicas/tratamento farmacológico , Animais , Apoptose/efeitos dos fármacos , Catequina/farmacologia , Catequina/uso terapêutico , Glutationa Peroxidase/metabolismo , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Malondialdeído/metabolismo , Aprendizagem em Labirinto/efeitos dos fármacos , Memória/efeitos dos fármacos , Transtornos da Memória/induzido quimicamente , Transtornos da Memória/metabolismo , Fármacos Neuroprotetores/farmacologia , Síndromes Neurotóxicas/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ratos Wistar , Superóxido Dismutase/metabolismo
2.
J Neurosci Rural Pract ; 4(2): 164-70, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23914093

RESUMO

INTRODUCTION: Transient global ischemia induces selective, delayed neuronal death of pyramidal neurons in the hippocampal CA1. Oxidative Stress is considered to be involved in a number of human diseases including ischemia. Preliminary studies confirmed reduction of cell death in brain following treatment with antioxidants. AIM: According to this finding, we study the relationship between consumption of olive oil on cell death and memory disorder in brain ischemia. We studied the protective effect of olive oil against ischemia-reperfusion. MATERIAL AND METHODS: EXPERIMENTAL DESIGN INCLUDES THREE GROUPS: Intact (n = 8), ischemic control (n = 8) and treatment groups with olive oil (n = 8). The mice treated with olive oil as pre-treatment for a week. Then, ischemia induced by common carotid artery ligation and following the reduction of inflammation [a week after ischemia], the mice post-treated with olive oil. Nissl staining applied for counting necrotic cells in hippocampus CA1. Tunnel kit was used to quantify apoptotic cell death while to short term memory scale, we apply y-maze and shuttle box tests and for detection the rate of apoptotic and treated cell, we used western blotting test for bax and bcl2 proteins. RESULTS: High rate of apoptosis was seen in ischemic group that significantly associated with short-term memory loss. Cell death was significantly lower when mice treated with olive oil. The memory test results were adjusted with cell death results and bax and bcl2 expression in all groups' comparison. Ischemia for 15 min induced cell death in hippocampus with more potent effect on CA1. CONCLUSION: Olive oil intake significantly reduced cell death and decreased memory loss.

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