Effect of Tiantai No.1 (天泰1号) on β-Amyloid-induced Neurotoxicity and NF-κ B and cAMP Responsive Elem

来源 :Chinese Journal of Integrative Medicine | 被引量 : 0次 | 上传用户:wang3398218
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Objective:To investigate the effect and molecular mechanism of Tiantai No.1(天泰1号),a compound Chinese herbal preparation,for the prevention and reduction of neurotoxicity induced by beta- amyloid peptides(Abeta)in vitro and its effects on nuclear factor-κB(NF-κB)and cAMP responsive element-binding protein(CREB)pathways using the gene transfection technique.Methods:B104 neuronal cells were used to examine the effects of Tiantai No.1 on lowering the neurotoxicity induced by Abeta.The cells were pre-treated with Tiantai No.1 at doses of 50,100,150,or 200μg/mL respectively for 3 days and co-treated with Tiantai No.1 and beta-amyloid peptidel-40(Aβ1-40,10μmol/L)for 48 h or post- treated with Tiantai No.1 for 48 h after the cells were exposed to beta-amyloid peptides25-35(Aβ25-35) for 8 h.In gene transfection assays,cells were treated with Tiantai No.1 at 50μg/mL and 150μg/mL for 5 days or co-treated with Tiantai No.1 and Aβ1-40(5μmo/L)for 3 days after electroporation for the evaluation of NF-κB and CREB expression.Results:Pre-treating and co-treating B104 neuronal cells with Tiantai No.1 lowered the neurotoxicity induced by Abeta,and post-treating with Tiantai No.1 reduced or blocked B104 neuronal apoptotic death induced by Abeta(P<0.05,P<0.01).With a dose-dependent relationship,the same treatments increased the expression of NF-κB or CREB in B104 neuronal cells (P<0.05,P<0.01).Meanwhile,Tiantai No.1 reduced Aβ-40 induced inhibition on NF-κB expression (P<0.01).Conclusions:Tiantai No.1 can protect neurons against the neurotoxicity induced by Abeta.The neuroprotective mechanisms may be associated with the activation of NF-κB and cAMP cellular signal pathways. Objective: To investigate the effect and molecular mechanism of Tiantai No.1, a compound Chinese herbal preparation, for the prevention and reduction of neurotoxicity induced by beta- amyloid peptides(Abeta)in vitro and its effects on nuclear factor-κB(NF-κB) and cAMP responsive element-binding protein(CREB) pathways using the gene transfection technique.Methods:B104 neuronal cells were used to examine the effects of Tiantai No.1 on lowering the neurotoxicity induced by Abeta.The Cells were pre-treated with Tiantai No.1 at doses of 50,100,150,or 200μg/mL respectively for 3 days and co-treated with Tiantai No.1 and beta-amyloid peptidel-40(Aβ1-40,10μmol/L) for 48 h or post- treated with Tiantai No.1 for 48 h after the cells exposed to beta-amyloid peptides25-35(Aβ25-35) for 8 h.In gene transfection assays,cells were treated with Tiantai No.1 at 50μg/ mL and 150μg/mL for 5 days or co-treated with Tiantai No.1 and Aβ1-40(5μmo/L) for 3 days after electroporation for the Evaluation of NF-κB and CREB expression.Results:Pre-treating and co-treating B104 neuronal cells with Tiantai No.1 lowered the neurotoxicity induced by Abeta, and post-treating with Tiantai No.1 reduced or blocked B104 neuronal apoptotic death induced By Abeta (P<0.05, P<0.01). With a dose-dependent relationship, the same treatment increased the expression of NF-κB or CREB in B104 neuronal cells (P<0.05, P<0.01). Meanwhile, Tiantai No. 1Reduced Aβ-40 induced inhibition on NF-κB expression (P<0.01).Conclusions:Tiantai No.1 can protect neurons against the neurotoxicity induced by Abeta.The neuroprotective mechanisms may be associated with the activation of NF-κB and cAMP cellular Signal pathways.
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