OBJECTIVE:To observe the effects of Bushen Huoxue Yin(补肾活血饮,BSHXY) on nuclear transcription factor kappa B(NF-κB) and nitric oxide(NO) in the brain of the Parkinson's disease(PD) model mouse.METHODS:Forty-fi...OBJECTIVE:To observe the effects of Bushen Huoxue Yin(补肾活血饮,BSHXY) on nuclear transcription factor kappa B(NF-κB) and nitric oxide(NO) in the brain of the Parkinson's disease(PD) model mouse.METHODS:Forty-five C57BL/6 mice were randomly divided into three groups;normal,model and BSHXY treatment groups.Concentrations of NF-κB and NO in mouse brain tissue were determined by ELISA and spectrophotometry,respectively.RESULTS:NF-κB concentration in brain tissue in the model group was 14.04±4.38 μg· L-1,which was higher than that in normal(P<0.01) and BSHXY(P< 0.05) groups.NO content in brain tissue in the model group was 5.93±0.79 μmol · gprot-1,which was also higher than that in model(P<0.01) and BSHXY(P<0.01) groups.However,there were no significant differences in the content of NF-κB and NO between BSHXY and normal groups(P>0.05).CONCLUSION:The mechanism of BSHXY for treatment of PD is possibly related to inhibition ofNF-κB activation and decreased NO content in the brain.展开更多
基金Supported by National Natural Science Foundation (No.30672762)
文摘OBJECTIVE:To observe the effects of Bushen Huoxue Yin(补肾活血饮,BSHXY) on nuclear transcription factor kappa B(NF-κB) and nitric oxide(NO) in the brain of the Parkinson's disease(PD) model mouse.METHODS:Forty-five C57BL/6 mice were randomly divided into three groups;normal,model and BSHXY treatment groups.Concentrations of NF-κB and NO in mouse brain tissue were determined by ELISA and spectrophotometry,respectively.RESULTS:NF-κB concentration in brain tissue in the model group was 14.04±4.38 μg· L-1,which was higher than that in normal(P<0.01) and BSHXY(P< 0.05) groups.NO content in brain tissue in the model group was 5.93±0.79 μmol · gprot-1,which was also higher than that in model(P<0.01) and BSHXY(P<0.01) groups.However,there were no significant differences in the content of NF-κB and NO between BSHXY and normal groups(P>0.05).CONCLUSION:The mechanism of BSHXY for treatment of PD is possibly related to inhibition ofNF-κB activation and decreased NO content in the brain.
