WU Zheng-zhi, Huang Andrew C J, de Vellis Jean, LI Ying-hong
Shenzhen Institute of Integrated Traditional and Western Medicine (Shenzhen), 518035, China.
Chin J Integr Med. 2008 Dec;14(4):286-92. doi: 10.1007/s11655-008-0286-y. Epub 2008 Dec 12.
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-kappa B (NF-kappa B) and cAMP responsive element-binding protein (CREB) pathways using the gene transfection technique.
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 200 micro g/mL respectively for 3 days and co-treated with Tiantai No.1 and beta-amyloid peptide1-40 (A beta 1-40, 10 micro mol/L) for 48 h or post-treated with Tiantai No.1 for 48 h after the cells were exposed to beta-amyloid peptides25-35 (A beta 25-35) for 8 h. In gene transfection assays, cells were treated with Tiantai No.1 at 50 micro g/mL and 150 micro g/mL for 5 days or co-treated with Tiantai No.1 and A beta 1-40 (5 micro mo/L) for 3 days after electroporation for the evaluation of NF-kappa B and CREB expression.
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-kappa B or CREB in B104 neuronal cells (P<0.05, P<0.01). Meanwhile, Tiantai No.1 reduced A beta -40 induced inhibition on NF-kappa B expression (P<0.01).
Tiantai No.1 can protect neurons against the neurotoxicity induced by Abeta. The neuroprotective mechanisms may be associated with the activation of NF-kappa B and cAMP cellular signal pathways.
运用基因转染技术，研究复方中药制剂天台一号在体外预防和减轻β-淀粉样肽（Aβ）诱导的神经毒性的作用及分子机制，以及其对核因子-κB（NF-κB）和环磷酸腺苷反应元件结合蛋白（CREB）信号通路的影响。
采用B104神经元细胞检测天台一号降低Aβ诱导的神经毒性的作用。细胞分别用50、100、150或200μg/mL剂量的天台一号预处理3天，然后与天台一号和β-淀粉样肽1-40（Aβ1-40，10μmol/L）共同处理48小时；或者在细胞暴露于β-淀粉样肽25-35（Aβ25-35）8小时后，用天台一号后处理48小时。在基因转染实验中，细胞用50μg/mL和150μg/mL的天台一号处理5天，或者在电穿孔后与天台一号和Aβ1-40（5μmol/L）共同处理3天，以评估NF-κB和CREB的表达。
天台一号预处理和共同处理B104神经元细胞可降低Aβ诱导的神经毒性，天台一号后处理可减少或阻断Aβ诱导的B104神经元凋亡死亡（P<0.05，P<0.01）。相同处理以剂量依赖关系增加B104神经元细胞中NF-κB或CREB的表达（P<0.05，P<0.01）。同时，天台一号降低了Aβ40诱导的对NF-κB表达的抑制作用（P<0.01）。
天台一号可保护神经元免受Aβ诱导的神经毒性。其神经保护机制可能与NF-κB和环磷酸腺苷细胞信号通路的激活有关。
