OBJECTIVE: To study the protective effect of butylphthalide in a cell model of Alzheimer's disease(AD) induced by Aβ25-35 in Neuro 2a (N2a) cells. METHODS: N2a cells were divided into AD group, butylphthalide (NBP) group and control group. AD cell model was established by adding 20 µmol/L Aβ25-35 to cultured N2a cells. The cells in NBP group were treated with 0.1, 1, 10, or 100 µmol/L NBP 4 h prior to treatment with 20 µmol/L Aβ25-35. The cell viability were determined by MTT assay, the cell apoptotic rate were detected by AnnexinV-FITC flow cytometry, and the cell morphological changes were observed under inverted phase contrast microscope. The expression of TNF-α and IL-1β mRNA were determined by qRT-PCR. RESULTS: Compared with those in the control group, the number of adherent cells was significantly decreased, neurite structures were reduced, and the cell viability was decreased, while the apoptotic rate and expressions of TNF-α and IL-1β mRNA were increased in AD group (P<0.05). Compared with that in AD group, the number of adherent cells was increased in NBP group and the cell morphology was similar to the normal control cells. The cell viability of N2a cells was increased in NBP group with decreased apoptotic rate and expression of TNF-αand IL-1β mRNA (P<0.05). CONCLUSION: Butylphthalide can protect against AD in the cell model induced by Aβ25-35 possibly by inhibiting the expression of inflammatory cytokines.
OBJECTIVE: To study the protective effect of butylphthalide in a cell model of Alzheimer's disease(AD) induced by Aβ25-35 in Neuro 2a (N2a) cells. METHODS: N2a cells were divided into AD group, butylphthalide (NBP) group and control group. AD cell model was established by adding 20 µmol/L Aβ25-35 to cultured N2a cells. The cells in NBP group were treated with 0.1, 1, 10, or 100 µmol/L NBP 4 h prior to treatment with 20 µmol/L Aβ25-35. The cell viability were determined by MTT assay, the cell apoptotic rate were detected by AnnexinV-FITC flow cytometry, and the cell morphological changes were observed under inverted phase contrast microscope. The expression of TNF-α and IL-1β mRNA were determined by qRT-PCR. RESULTS: Compared with those in the control group, the number of adherent cells was significantly decreased, neurite structures were reduced, and the cell viability was decreased, while the apoptotic rate and expressions of TNF-α and IL-1β mRNA were increased in AD group (P<0.05). Compared with that in AD group, the number of adherent cells was increased in NBP group and the cell morphology was similar to the normal control cells. The cell viability of N2a cells was increased in NBP group with decreased apoptotic rate and expression of TNF-αand IL-1β mRNA (P<0.05). CONCLUSION:Butylphthalide can protect against AD in the cell model induced by Aβ25-35 possibly by inhibiting the expression of inflammatory cytokines.
Authors: Kathryn P MacPherson; Pradoldej Sompol; George T Kannarkat; Jianjun Chang; Lindsey Sniffen; Mary E Wildner; Christopher M Norris; Malú G Tansey Journal: Neurobiol Dis Date: 2017-02-24 Impact factor: 5.996
Authors: Ingrid H Philippens; Paul R Ormel; Guus Baarends; Maja Johansson; Ed J Remarque; Magnus Doverskog Journal: J Alzheimers Dis Date: 2017 Impact factor: 4.472