title: β-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkA NGFR.
abstract: 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.
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
authors.forename: Jun-Feng
authors.initials: JF
authors.lastname: Li
authors.forename: Jian-Chang
authors.initials: JC
authors.lastname: Shu
authors.forename: Shao-Hui
authors.initials: SH
authors.lastname: Tang
authors.forename: Yan-Mei
authors.initials: YM
authors.lastname: Deng
authors.forename: Mei-Ya
authors.initials: MY
authors.lastname: Fu
authors.forename: Xia
authors.initials: X
authors.lastname: Lv
mesh_terms: D000906:Antibodies / Q000276:immunology; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D049109:Cell Proliferation; D005688:Galactosamine / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D022781:Hepatocytes / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D020932:Nerve Growth Factor / Q000235:genetics / Q000276:immunology / Q000494:pharmacology*; D020800:Receptor, Nerve Growth Factor / Q000378:metabolism; D020917:Receptor, trkA / Q000276:immunology / Q000378:metabolism*; D011994:Recombinant Proteins / Q000096:biosynthesis / Q000276:immunology / Q000494:pharmacology; D012709:Serum Albumin / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000906:Antibodies; D020800:Receptor, Nerve Growth Factor; D011994:Recombinant Proteins; D012709:Serum Albumin; D008315:Malondialdehyde; D005688:Galactosamine; D020932:Nerve Growth Factor; D007770:L-Lactate Dehydrogenase; D020917:Receptor, trkA; D005978:Glutathione