Chinese Journal of Integrative Medicine

, Volume 14, Issue 4, pp 286–292

Effect of Tiantai No.1 (天泰1号) on β-amyloid-induced neurotoxicity and NF-κ B and cAMP responsive element-binding protein

  • Zheng-zhi Wu (吴正治)
  • Andrew C. J. Huang
  • Jean de Vellis
  • Ying-hong Li (李映红)
Experimental Research

DOI: 10.1007/s11655-008-0286-y

Cite this article as:
Wu, Z., Huang, A.C.J., de Vellis, J. et al. Chin. J. Integr. Med. (2008) 14: 286. doi:10.1007/s11655-008-0286-y



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-κ B (NF-κ 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 μ g/mL respectively for 3 days and co-treated with Tiantai No.1 and beta-amyloid peptide1–40 (A β 1–40, 10 μ 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 β 25–35) for 8 h. In gene transfection assays, cells were treated with Tiantai No.1 at 50 μ g/mL and 150 μ g/mL for 5 days or co-treated with Tiantai No.1 and A β 1–40 (5 μ mo/L) for 3 days after electroporation for the evaluation of NF-κ 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-κ B or CREB in B104 neuronal cells (P<0.05, P<0.01). Meanwhile, Tiantai No.1 reduced A β -40 induced inhibition on NF-κ 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-κ B and cAMP cellular signal pathways.

Key Words

Alzheimer’s disease beta-amyloid peptide apoptosis nuclear factor-κ B cAMP responsive element-binding protein Tiantai No.1 

Copyright information

© Chinese Association of the Integration of Traditional and Western Medicine and Springer-Verlag GmbH 2008

Authors and Affiliations

  • Zheng-zhi Wu (吴正治)
    • 1
  • Andrew C. J. Huang
    • 2
  • Jean de Vellis
    • 3
  • Ying-hong Li (李映红)
    • 1
  1. 1.Shenzhen Institute of Integrated Traditional and Western MedicineShenzhenChina
  2. 2.Department of Medicine, Division of Endocrinology, Larry Hillblom Islet Research Center, David Geffen School of MedicineUCLALos AngelesUSA
  3. 3.Department of Neurobiology, Mental Retardation Research CenterNeuropsychiatric Institute David Geffen School of Medicine at UCLALos AngelesUSA

Personalised recommendations