Protective Role of α2HS-Glycoprotein in HBV-Associated Liver Failure

International Journal of Molecular Sciences

Xia-Hong Dai²  Pan Zhang¹  Mei-Fang Xiao²  Rong-Rong Zhou²  Bao-Xin Zhang²  Guan-Sheng Hu²  Ze-Bing Huang² 

[1] Department of Infectious Diseases, The Third Affiliated Hospital of Xiangya, Central South University, Changsha, Hunan, 410008, China; E-Mail:;Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China; E-Mails:

关键词: human fetuin-a;    α2-Heremans-Schmid glycoprotein;    spermine;    acute-on-chronic liver failure;   

DOI  :  10.3390/ijms12063846

来源: mdpi

【 摘 要 】

In this study, levels of plasma α2-Heremans-Schmid glycoprotein, serum tumor necrosis factor-α, serum liver function parameters and short-term mortality were measured in 100 hepatitis B patients. Release of interleukin-6 and tumor necrosis factor-α from the lipopolysaccharide-stimulated peripheral blood mononuclear cells in the presence/absence of spermine and α2-Heremans-Schmid glycoprotein were analyzed by enzyme-linked immunosorbent assay to determine the significance and potential mechanism of α2-Heremans-Schmid glycoprotein in hepatitis B virus-associated liver damage. Results showed that serum α2-Heremans-Schmid glycoprotein levels in acute-on-chronic liver failure patients were significantly lower than that in chronic hepatitis B patients or healthy controls (p < 0.05). A negative dependence between serum human α2-Heremans-Schmid glycoprotein and tumor necrosis factor-α levels was observed. Interleukin-6 and tumor necrosis factor-α levels in the lipopolysaccharide-induced peripheral blood mononuclear cell supernates were significantly reduced by spermine and/or α2-Heremans-Schmid glycoprotein. The latter two proteins jointly inhibited cytokine release. These observations suggest that plasma α2-Heremans-Schmid glycoprotein is an independent marker of liver damage and a prognostic indicator of hepatitis B virus chronicity. It may reduce liver inflammation by partially inhibiting release of inflammatory factors from activated peripheral blood mononuclear cells.

【 授权许可】

CC BY   
© 2011 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.