Open Accessβ-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkANGFR
Author(s) -
Junfeng Li,
Jian-Chang Shu,
Shaohui Tang,
Yan-mei Deng,
Mei-ya Fu,
Xin Lv
Publication year - 2013
Publication title -
molecular medicine reports
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2013.1590
Subject(s) - nerve growth factor , tyrosine phosphorylation , microbiology and biotechnology , low affinity nerve growth factor receptor , receptor tyrosine kinase , hepatocyte growth factor receptor , biology , neurotrophin , cell growth , receptor , growth factor , hepatocyte growth factor , signal transduction , endocrinology , medicine , biochemistry , c met
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.