Protective effect of nicotine on the cultured rat basal forebrain neurons damaged by β-Amyloid (Aβ)25-35 protein cytotoxicity

C.-N. Guo, L. Sun, G.-L. Liu, S.-J. Zhao, W.-W. Liu, Y.-B. Zhao

Department of Neurology, The Shanghai First People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China. zyb62@medmail.com.cn

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• Neurology

OBJECTIVE: We sought to investigate the intervention effect of nicotine on β-amyloid (Aβ)25-35 protein cytotoxicity in the rat basal forebrain neurons primary cultures.

MATERIALS AND METHODS: For this purpose, freshly isolated rat basal forebrain neurons were cultured for 7 days and then exposed to either Aβ(25-35) or the combination of Aβ(25-35) and nicotine for 48 hours. The effects of Aβ(25-35) and nicotine on neurons morphology, growth status and TrkA expression were evaluated through microscopy, MTT assay, RT-PCR and immunocytochemistry.

RESULTS: We found that the exposure of cultured neurons to Aβ(25-35) resulted in remarkable morphological changes. The average process number and length as well as the maximum process length of neurons were significantly decreased as compared with those of control. MTT assay showed that Aβ(25-35) impaired the growth of neurons. Aβ(25-35) also inhibited the expression of TrkA at both mRNA and protein levels. However, the addition of nicotine significantly attenuated these changes, indicating that nicotine could protect the neurons from the cytotoxicity of Aβ(25-35).

CONCLUSIONS: Nicotine could be useful for the treatment of Alzheimer’s disease through its ability to rescue the neurons from Aβ(25-35) cytotoxicity and the protective effect involved upregulated expression of TrkA receptors.

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