【预售 按需印刷】Neuropharmacological & Biochemical Evaluation for Schizophrenia
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书名:Neuropharmacological & Biochemical Evaluation for Schizophrenia
定价:1008.0
ISBN:9783659346330
作者: Ashwlayan Vrish Dhwaj
版次:1
出版时间:2013-02
内容提要:
Schizophrenia a chronic, debilitating psychiatric disorder comprises of positive and negative symptoms along with cognitive and attention impairments. Antipsychotic drugs available in the market for treatment of schizophrenia have either been unable to treat all the symptoms of schizophrenia or accompany a lot of side-effects. Ketamine, a NMDA receptor antagonist was used to model psychotic symptoms in mice. Herbal compounds (CDRB01 and CDRP01) normalized the ketamine induced increased NR1A protein expression, reduced acetylcholinesterase activity as well as monoamine oxidase activity but did not show any extrapyramidal side effects. Estimation of brain neurotransmitter level revealed that both compounds reduced DA and 5-HT content in the cortex, striatal and hippocampal regions. CDR-B01 was effective in ameliorating positive, negative as well as cognitive dysfunctions induced by ketamine. Whereas compound CDRP01 significantly attenuated ketamine induced increased D1 receptor expression but had no significant effects on D2 expression, showed efficacy in the negative and cognitive symptoms only. They normalized GSH level, reduced lipid peroxidation & nitrite but increased SOD level.
定价:1008.0
ISBN:9783659346330
作者: Ashwlayan Vrish Dhwaj
版次:1
出版时间:2013-02
内容提要:
Schizophrenia a chronic, debilitating psychiatric disorder comprises of positive and negative symptoms along with cognitive and attention impairments. Antipsychotic drugs available in the market for treatment of schizophrenia have either been unable to treat all the symptoms of schizophrenia or accompany a lot of side-effects. Ketamine, a NMDA receptor antagonist was used to model psychotic symptoms in mice. Herbal compounds (CDRB01 and CDRP01) normalized the ketamine induced increased NR1A protein expression, reduced acetylcholinesterase activity as well as monoamine oxidase activity but did not show any extrapyramidal side effects. Estimation of brain neurotransmitter level revealed that both compounds reduced DA and 5-HT content in the cortex, striatal and hippocampal regions. CDR-B01 was effective in ameliorating positive, negative as well as cognitive dysfunctions induced by ketamine. Whereas compound CDRP01 significantly attenuated ketamine induced increased D1 receptor expression but had no significant effects on D2 expression, showed efficacy in the negative and cognitive symptoms only. They normalized GSH level, reduced lipid peroxidation & nitrite but increased SOD level.
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