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INTRODUCTION: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a decrement in the number of synapses, an increment in the production of oxygen free radicals and inflammatory cytokines. Green tea (GT) plays a defensive performance in different neurodegenerative conditions, such as cognition deficit. This study investigated the neuroprotective effect of green tea (GT) on cognitive disorder, inflammation, and oxidative stress in the streptozotocin (STZ)- induced AD model. MATERIALS AND METHODS: The rats were divided into four groups: (1) Control, (2) GT, (3) Alz, and (4) GT + Alz. AD was induced by the injection of STZ (3 mg/kg, bilaterally, ICV). Morris water maze and passive avoidance tests were done to evaluate the memory and learning of rats. Biochemical parameters were measured with specialized ELISA kits. RESULTS: Briefly, data analysis revealed that GT administration for 21 days improved memory impairment induced by the injection of STZ. Pretreatment with GT enhanced time spent in the goal quarter and reduced latency time and path length. Furthermore, pretreatment with GT prevented the increment of malondialdehyde (MDA) concentration in STZ-treated rats. As a pro-inflammatory cytokine, tumor necrosis factor- α (TNF-α) concentration was suppressed with the GT pretreatment. Total antioxidant capacity was increased after GT administration in rats treated compared with AD rats. CONCLUSIONS: GT pretreatment attenuated STZ-induced learning and memory impairment through the suppression of TNF-α and MDA concentrations. The beneficial effects of GT on memory could be attributed to its protective effects on oxidative defenses.
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Enfermedad de Alzheimer , Disfunción Cognitiva , Fármacos Neuroprotectores , Ratas , Animales , Enfermedad de Alzheimer/tratamiento farmacológico , Aprendizaje por Laberinto , Factor de Necrosis Tumoral alfa , Té , Ratas Wistar , Modelos Animales de Enfermedad , Disfunción Cognitiva/tratamiento farmacológico , Disfunción Cognitiva/prevención & control , Estreptozocina , Estrés Oxidativo , Trastornos de la Memoria/inducido químicamente , Fármacos Neuroprotectores/uso terapéutico , Citocinas/metabolismoRESUMEN
OBJECTIVE: Quercetin is one of the most popular flavonoid with protective effects against neural damages in Parkinson's disease (PD). We assessed the effect of quercetin administration on memory and motor function, hippocampal oxidative stress and brain-derived neurotrophic factor (BDNF) level in a 6-OHDA-induced Parkinson's rat model. MATERIAL AND METHODS: The animals were divided into the following five groups (n=8): control, sham-surgery (sham), lesion (PD), and lesion animals treated with quercetin at doses of 10 (Q10) and 25 (Q25) mg/kg. For induction of a model of PD, 6-OHDA was injected into the striatum of rats. The effects of quercetin were investigated on spatial memory, hippocampal BDNF and malondialdehyde (MDA) levels, and total antioxidant capacity (TAC). Spatial memory was assessed by Morris water maze test, and the neuronal firing frequency in hippocampal dentate gyrus (HDG) was evaluated by single-unit recordings. RESULTS: Mean path length and latency time, rotational behavior and hippocampal MDA concentration were significantly increased, while time spent in the goal quadrant, swimming speed, spike rate, and hippocampal levels of TAC and BDNF were significantly decreased in the PD group compared to the sham group (p<0.01 to p<0.001). Quercetin treatment significantly enhanced time spent in goal quadrant (p<0.05), swimming speed (p<0.001) and spike rate (p<0.01), improved hippocampal TAC (p<0.05 to p<0.001) and BDNF (p<0.01 to p<0.001) level, and decreased mean path length (p<0.001), latency time (p<0.05 to p<0.001), rotational behavior and hippocampal MDA concentration (p<0.05). CONCLUSION: The cognitive-enhancing effect of quercetin might be due to its antioxidant effects in the hippocampus.
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In patients with multiple sclerosis (MS) disease, cognitive deficits have been detected because of destruction of hippocampus. Cognitive impairment is one of the common signs in MS. Recent studies showed that metformin (Met) has wide-ranging effects in the treatment of diseases. Here, we have tried to study the preservative effects of Met as adenosine monophosphate-activated protein kinase (AMPK) activator on the hippocampus dentate gyrus (DG) neuronal firing pattern, motor coordination, and learning & memory loss following MS induction. The MS induction was done by local ethidium bromide (EB) injection into the rat hippocampus. Then, rats were treated with Met (200 mg/kg) for two weeks. Spatial memory and learning status were assessed using Morris water maze. A neuronal single-unit recording was measured from hippocampus DG. After decapitation, the bilateral hippocampi separated to measure malondialdehyde (MDA). Treatment with Met ameliorated latency times and path lengths (P < 0.05, P < 0.01, P < 0.001 in 1th, 2th, 3th and 4th days) in the Met + MS group respectively. The percent of total time spent in goal quarter and the average number of spikes/bin were decreased significantly in MS rats compared with the sham group (p < 0.001) but significantly increased in the metformin-treated MS group (Met + MS), (p < 0.01, p < 0.001). Met treatment in rats with MS significantly reduced the concentration of MDA, which is an indicator of lipid peroxidation compared to untreated groups. These observations show that increase of neuronal activity, sensory-motor coordination, and improvement of spatial memory in MS rats treated with Met appears via an increment of AMPK.
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Proteínas Quinasas Activadas por AMP/metabolismo , Metformina/uso terapéutico , Esclerosis Múltiple/tratamiento farmacológico , Esclerosis Múltiple/enzimología , Aprendizaje Espacial/efectos de los fármacos , Memoria Espacial/efectos de los fármacos , Animales , Modelos Animales de Enfermedad , Evaluación Preclínica de Medicamentos/métodos , Activación Enzimática/efectos de los fármacos , Activación Enzimática/fisiología , Hipocampo/efectos de los fármacos , Hipocampo/enzimología , Masculino , Metformina/farmacología , Ratas , Ratas Wistar , Aprendizaje Espacial/fisiología , Memoria Espacial/fisiología , Resultado del TratamientoRESUMEN
OBJECTIVES: In this study the effect of oral administration of honey on serum glucose, lipids, stress oxidative markers, and morphology of langerhans islets in noise induced hyperglycemic rats was investigated. MATERIALS AND METHODS: Male Wistar rats were divided into control, hyperglycemic, honey treated control, and honey treated hyperglycemic groups. For induction of hyperglycemia, noise stress was used. Serum glucose, triglyceride (TG), total cholesterol, low density lipoprotein (LDL), and high density lipoprotein (HDL)-cholesterol levels were determined before the study and at 4(th) and 8(th) weeks after the study. Markers of oxidative stress in brain were also measured. Morphology of langerhans islets in four groups was evaluated using Gomori staining method. RESULTS: Treatment of noise induced hyperglycemic rats with honey produced a hypoglycemic effect and appropriate changes regarding serum lipids in treated diabetic group at 4(th) and 8(th) weeks as compared to the control group. Meanwhile, honey treatment significantly ameliorated the increased malondialdehyde (MDA) content and reduced the activity of superoxide dismutase (SOD) in brain. Histology of langerhans islets in hyperglycemic group showed a lower number and granularity of beta cells; honey treatment produced beneficial change in this respect. CONCLUSION: Oral administration of honey in experimental model of diabetes showed a significant hypoglycemic effect and led to appropriate changes in serum lipid profiles.