β-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkANGFR

Li,Jun-Feng; Shu,Jian-Chang; Tang,Shao-Hui; Deng,Yan-Mei; Fu,Mei-Ya; Lv,Xia

doi:10.3892/mmr.2013.1590

September 2013 Volume 8 Issue 3

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September 2013 Volume 8 Issue 3

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Article

β-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkANGFR

Authors:
- Jun-Feng Li
- Jian-Chang Shu
- Shao-Hui Tang
- Yan-Mei Deng
- Mei-Ya Fu
- Xia Lv
View Affiliations / Copyright

Affiliations: Department of Gastroenterology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China, Department of Gastroenterology, The Fourth Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510175, P.R. China
Pages: 813-817
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Published online on: July 16, 2013

https://doi.org/10.3892/mmr.2013.1590
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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 (TrkANGFR) 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-TrkANGFR 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/TrkANGFR signaling pathway.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

β-Nerve growth factor attenuates hepatocyte injury induced by D-galactosamine in vitro via TrkANGFR

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