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1.
Pak J Pharm Sci ; 33(6(Supplementary)): 2785-2791, 2020 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-33879438

RESUMEN

Exposure to cadmium has been extensively increased due to its usage in modern daily life. Inside the human body it induces deteriorating effects in every vital organ including brain. Oxidative stress has been widely implicated in neurotoxicity induced by cadmium exposure. Consumption of dietary source of exogenous antioxidants is one of the recommended ways to extenuate heavy metal-induced oxidative stress. The potential of nuts against heavy-metal induced neurotoxicity has not been investigated earlier. This study was, therefore, conducted to find out the antioxidant ability of almond and walnut in the prevention of cadmium-induced oxidative stress. Rats were treated with nuts (400 mg/kg) daily for 28 days whereas, cadmium (50 mg/kg) was given once in a week. Brain function was monitored in terms of memory performance using Morris water maze and elevated plus maze. Moreover, oxidative stress status was also evaluated. Results showed that weekly exposure of cadmium significantly reduced %memory retention, increased lipid per oxidation and inhibited antioxidant enzymes activity. When nuts supplemented rats were monitored for these parameters, it was observed that almond and walnut have a great potential to reduce cadmium-induced neurotoxicity as evident by decreased oxidative stress and improved memory function in cadmium intoxicated rats.


Asunto(s)
Antioxidantes/farmacología , Encéfalo/efectos de los fármacos , Cadmio/toxicidad , Juglans , Estrés Oxidativo/efectos de los fármacos , Prunus dulcis , Animales , Catalasa/metabolismo , Suplementos Dietéticos , Glutatión Peroxidasa/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Masculino , Memoria/efectos de los fármacos , Ratas , Ratas Wistar , Superóxido Dismutasa/metabolismo
2.
Pak J Pharm Sci ; 32(4(Supplementary)): 1893-1900, 2019 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-31680089

RESUMEN

Unpredictable chronic mild stress (UCMS) model is the most established method to study neurobiological mechanisms of depression. This work was intended to explore the efficacy of curcumin to revert the UCMS-induced oxidative burden and associated depression as well as potential of curcumin as an acetyl cholinesterase (AchE) inhibitor. Animals were initially grouped into control and curcumin (200mg/kg, p.o) and further subdivided into unstressed and stressed groups. Depression and anxiety were evaluated by forced swim test (FST) and light/dark transition (LDT) while memory function was assessed by passive avoidance test (PAT). Effect of curcumin on oxidative stress following UCMS was determined by measuring peroxidation of lipid (LPO) and antioxidant enzyme activities. AchE activity was also determined. Findings showed that curcumin supplementation significantly attenuated the UCMS-induced depression and anxiety like symptoms, decreased the load of UCMS propagated oxidative stress by improving antioxidant enzymes activities. Curcumin also improved the memory function and exhibited inhibitory effect on AchE activity. In conclusion it can be suggested that supplementation of curcumin in daily life can help in combating the stress-induced depression and ever increasing load of oxidative stress. Study also highlights the anti-acetylcholinesterase potential of curcumin which may be responsible for improved memory function following UCMS.


Asunto(s)
Acetilcolinesterasa/metabolismo , Inhibidores de la Colinesterasa/farmacología , Curcumina/farmacología , Depresión/tratamiento farmacológico , Trastornos de la Memoria/tratamiento farmacológico , Estrés Oxidativo/efectos de los fármacos , Estrés Psicológico/tratamiento farmacológico , Animales , Antioxidantes/farmacología , Ansiedad/tratamiento farmacológico , Ansiedad/metabolismo , Depresión/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Masculino , Aprendizaje por Laberinto/efectos de los fármacos , Memoria/efectos de los fármacos , Trastornos de la Memoria/metabolismo , Ratones , Ratas Wistar , Estrés Psicológico/metabolismo
3.
Brain Res Bull ; 120: 63-74, 2016 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-26548495

RESUMEN

Dietary nutrients may play a vital role in protecting the brain from age-related memory dysfunction and neurodegenerative diseases. Tree nuts including almonds have shown potential to combat age-associated brain dysfunction. These nuts are an important source of essential nutrients, such as tocopherol, folate, mono- and poly-unsaturated fatty acids, and polyphenols. These components have shown promise as possible dietary supplements to prevent or delay the onset of age-associated cognitive dysfunction. This study investigated possible protective potential of almond against scopolamine induced amnesia in rats. The present study also investigated a role of acetylcholine in almond induced memory enhancement. Rats in test group were orally administrated with almond suspension (400 mg/kg/day) for four weeks. Both control and almond-treated rats were then divided into saline and scopolamine injected groups. Rats in the scopolamine group were injected with scopolamine (0.5 mg/kg) five minutes before the start of each memory test. Memory was assessed by elevated plus maze (EPM), Morris water maze (MWM) and novel object recognition (NOR) task. Cholinergic function was determined in terms of hippocampal and frontal cortical acetylcholine content and acetylcholinesterase activity. Results of the present study suggest that almond administration for 28 days significantly improved memory retention. This memory enhancing effect of almond was also observed in scopolamine induced amnesia model. Present study also suggests a role of acetylcholine in the attenuation of scopolamine induced amnesia by almond.


Asunto(s)
Trastornos de la Memoria/dietoterapia , Prunus dulcis , Acetilcolina/metabolismo , Acetilcolinesterasa/metabolismo , Animales , Modelos Animales de Enfermedad , Lóbulo Frontal/metabolismo , Hipocampo/metabolismo , Aprendizaje por Laberinto , Trastornos de la Memoria/metabolismo , Distribución Aleatoria , Ratas Wistar , Reconocimiento en Psicología , Escopolamina , Resultado del Tratamiento
4.
Life Sci ; 124: 110-9, 2015 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-25637686

RESUMEN

AIMS: D-Galactose (D-gal) induced accelerated senescence has been used to develop an aging model for brain. Previously, long term administration of a wide range of doses has been used for this purpose. In the present study we investigate whether short term administration of a high dose of D-gal in rats induces significant signs and symptoms similar to natural aging. MAIN METHODS: Young rats were injected intraperitoneally with D-gal at a dose of 300 mg/ml/kg for one week. Behavioral analysis for depression and anxiety like symptoms were monitored by forced swim test (FST) and light/dark transition (LDT) test. Assessment of memory was done using the Morris water maze (MWM), passive avoidance test (PAT) and elevated plus maze (EPM) test. Biochemical analysis was done for estimation of antioxidant enzymes and acetylcholinesterase. Determination of brain biogenic amines was performed by HPLC-EC. KEY FINDINGS: Short term administration of D-gal significantly altered behavioral, biochemical and neurochemical responses in rats. D-Gal injected rats exhibited depressogenic and anxiogenic behaviors while memory was also significantly impaired in these rats. Brain lipid peroxidation and superoxide dismutase activity were significantly increased while catalase and glutathione peroxidase decreased. Increased activity of acetylcholinesterase was also exhibited by D-gal injected rats while brain biogenic amines were significantly decreased. Food intake and growth rate were however comparable in both groups. SIGNIFICANCE: Together the behavioral, biochemical and neurochemical impairments following the high dose of D-gal suggest that symptoms similar to natural aging may be developed in rats in as early as one week.


Asunto(s)
Envejecimiento/fisiología , Conducta Animal/fisiología , Encéfalo/fisiología , Galactosa/farmacología , Memoria/fisiología , Acetilcolinesterasa/metabolismo , Animales , Antioxidantes/metabolismo , Aminas Biogénicas/metabolismo , Catalasa/metabolismo , Cromatografía Líquida de Alta Presión , Relación Dosis-Respuesta a Droga , Galactosa/administración & dosificación , Glutatión Peroxidasa/metabolismo , Peroxidación de Lípido/fisiología , Masculino , Aprendizaje por Laberinto , Ratas , Ratas Wistar , Factores de Tiempo
5.
Plant Foods Hum Nutr ; 66(4): 335-40, 2011 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-22048906

RESUMEN

Walnut has been regarded as a health food that is delicious and nutritious. Both preventive and therapeutic effects of walnut are well documented. Walnuts are rich in omega-3 fatty acids that are reported to have beneficial effects on brain function. The present work was designed to evaluate the effects of walnuts on learning and memory in male rats. The effect of oral intake of walnut was also monitored on food intake. Walnut was given orally to rats for a period of 28 days. Memory function in rats was assessed by elevated plus maze (EPM) and radial arm maze (RAM). A significant improvement in learning and memory of walnut treated rats compared to controls was observed. Walnut treated rats also exhibited a significant decrease in food intake while the change in growth rate (in terms of percentage) remained comparable between the two groups. Analysis of brain monoamines exhibited enhanced serotonergic levels in rat brain following oral intake of walnuts. The findings suggest that walnut may exert its hypophagic and nootropic actions via an enhancement of brain 5-HT metabolism.


Asunto(s)
Juglans/química , Aprendizaje por Laberinto/efectos de los fármacos , Memoria/efectos de los fármacos , Nootrópicos/farmacología , Administración Oral , Animales , Peso Corporal/efectos de los fármacos , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Ingestión de Alimentos/efectos de los fármacos , Masculino , Sistema Nervioso/química , Sistema Nervioso/efectos de los fármacos , Ratas , Ratas Wistar , Serotonina/análisis , Serotonina/metabolismo , Triptófano/análisis , Triptófano/metabolismo
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