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Role of ERK/CREB signal pathway in promotion of BDNF expression in Aβ intoxicated SH-SY5Y cells by smilagenin

ZHANG Rui1, 2, XIA Zhi-ming1, SUN Xiao-yu1, Li Jia-mei1, ZHANG Yong-fang1, 2, HU Ya-er1, 2   

  1. 1.Research Laboratory of Cell Regulation, 2.Collaborative Innovation Center for Translational Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Online:2016-05-28 Published:2016-05-26
  • Supported by:

    Shanghai Municipal Health Bureau Foundation，20124y007；National Natural Science Foundation of China， 81573401

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Abstract:

Objective To investigate the role of extracellular signal regulated kinase/cAMP response element binding protein (ERK/CREB) signaling pathway in promotion of brain derived neurotrophic factor (BDNF) expression in β-amyloid (Aβ) intoxicated SH-SY5Y cells by smilagenin (SMI) and relevant mechanisms. Methods The Aβ intoxicated cell model was built and RT-PCR assay was employed to detect the BDNF mRNA expression. Western blotting was used to detect changes in pCREB and pERK expressions. Finally, the role of ERK/CREB signaling pathway in the promotion of BDNF mRNA expression by SMI was confirmed by the use of blocking assay. Results SMI promoted the BDNF mRNA expression in Aβ intoxicated SH-SY5Y cells (P=0.000) and up-regulated the phosphorylation level of signal molecules CREB and ERK1/2 (P=0.001, P=0.000). After blocking the CREB expression by RNA interference, the effect of SMI on promoting the BDNF mRNA expression completely vanished. After blocking the ERK1/2 phosphorylation with U0126, the effect of SMI on promoting the increase in pCREB level completely vanished. Conclusion SMI promotes the BDNF mRNA expression in Aβ intoxicated SH-SY5Y cells through the ERK/CREB pathway.

Key words: smilagenin, Alzheimers disease, brain-derived neurotrophic factor, cAMP response element binding protein, extracellular signal-regulated kinase