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Effect of Tiantai No.1 on beta-amyloid-induced neurotoxicity and NF-kappa B and cAMP responsive element-binding
Zheng-zhi WU1, Andrew C J Huang, Jean de Vellis
1Shenzhen Institute of Integrated Traditional and Western Medicine (Shenzhen), 518035, China. zhengzhw@yahoo.com.cn
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-kappa B (NF-kappa B) 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 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.
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-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).
Conclusions:
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.
Insights
Tiantai No.1 protects neurons from beta-amyloid peptide neurotoxicity by activating nuclear factor-kappa B (NF-kappa B) and cAMP responsive element-binding protein (CREB) pathways. This compound herbal preparation offers a potential therapeutic strategy for neurodegenerative conditions.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Beta-amyloid peptides (Abeta) are implicated in neurotoxicity and neuronal cell death.
- Understanding the molecular mechanisms underlying Abeta-induced neurotoxicity is crucial for developing effective interventions.
- Nuclear factor-kappa B (NF-kappa B) and cAMP responsive element-binding protein (CREB) are key signaling pathways involved in neuronal survival and function.
Purpose of the Study:
- To investigate the neuroprotective effects of Tiantai No.1 against Abeta-induced neurotoxicity in vitro.
- To elucidate the molecular mechanisms of Tiantai No.1, focusing on its impact on NF-kappa B and CREB pathways.
Main Methods:
- B104 neuronal cells were utilized to assess Tiantai No.1's effects on Abeta-induced neurotoxicity.
- Cells were pre-treated, co-treated, or post-treated with varying concentrations of Tiantai No.1 and Abeta peptides (Abeta1-40, Abeta25-35).
- Gene transfection assays were employed to evaluate the expression of NF-kappa B and CREB following Tiantai No.1 treatment.
Main Results:
- Tiantai No.1 pre-treatment, co-treatment, and post-treatment significantly reduced Abeta-induced neurotoxicity and apoptotic cell death.
- Tiantai No.1 demonstrated a dose-dependent increase in NF-kappa B and CREB expression.
- Tiantai No.1 counteracted the inhibitory effects of Abeta-40 on NF-kappa B expression.
Conclusions:
- Tiantai No.1 exhibits significant neuroprotective properties against Abeta-induced toxicity.
- The observed neuroprotection is potentially mediated by the activation of NF-kappa B and cAMP cellular signaling pathways.
- Tiantai No.1 represents a promising therapeutic candidate for conditions associated with Abeta neurotoxicity.
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