• DOI:10.3892/mmr.2013.1590
• Corpus ID: 20385659

β-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkA NGFR.

@article{Li2013NerveGF,
  title={$\beta$-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkA NGFR.},
  author={Jun-feng Li and Jian-chang Shu and Shao-Hui Tang and Yanrui Deng and Mei-ya Fu and Xia Lv},
  journal={Molecular medicine reports},
  year={2013},
  volume={8 3},
  pages={
          813-7
        }
}

• Jun-feng Li, J. Shu, +3 authors X. Lv
• Published 1 September 2013
• Biology
• Molecular medicine reports

Nerve growth factor (NGF) regulates the proliferation, differentiation and survival of cells and is also involved in the wound healing and tissue remodeling processes. The biological effects of NGF are dependent upon receptor signal-mediating functions, which differ between cells. This study attempted to investigate the hepatoprotective effect and possible mechanism of β-NGF on D-galactosamine (D-GalN)-injured human liver L-02 cell lines. We demonstrated that L-02 cells expressed the neurotrophin receptors tyrosine kinase-A nerve growth factor receptor (TrkA NGFR) and p75 pan-neurotrophin receptor (p75NTR). Recombinant human β-NGF markedly reduced cell injury and promoted the proliferation of L-02 cells damaged by D-GalN. However, this proliferation effect was blocked by the anti-TrkA NGFR antibody. Lactate dehydrogenase (LDH) and malondialdehyde (MDA) were released at reduced levels in the L-02 cell culture supernatant pretreated with β-NGF. Furthermore, the albumin (ALB) content in the cell medium and intracellular glutathione (GSH) levels were markedly augmented, and the permeability of the mitochondrial membrane of the L-02 cells was improved by β-NGF. Our results suggested that exogenous β-NGF protects L-02 cells from D-GalN-induced injury through the NGF/TrkA NGFR signaling pathway.