[Hypomethylation of TNF-alpha gene promoter in the patients with acute-on-chronic hepatitis B liver failure]

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2011 Oct;25(5):368-70.
[Article in Chinese]

Abstract

Objective: The present study was designed to investigate the possible epigenetic alteration in the promoter of TNF-alpha in the patients with acute-on-chronic hepatitis B liver failure (ACHBLF).

Methods: The methylation of TNF-alpha promoter in peripheral blood mononuclear cells (PBMCs) was measured by methylation specific PCR (MSP). The level of serum TNF-alpha was determined by enzyme-linked immunosorbent assay (ELISA). Model for End-stage Liver Disease (MELD) was performed for the evaluation of liver failure.

Results: The serum level of TNF-alpha in patients with ACHBLF(44.9260 +/- 26.48523) was higher than that in CHB (18.92505 +/- 9.04461) and healthy controls (11.9172 +/- 5.04612) (P < 0.05). Moreover, the serum TNF-alpha level was significantly decreased in methylation group as compared to unmethylaiton group in patients with ACHBLF (P < 0.05). MELD was not significantly different between methylated and unmethylated group of ACHBLF patients (P > 0.05). In addition, the serum level of TNF-alpha was found to be positively correlated with serum total bilirubin (r = 0.891, P < 0.01) and MELD score (r = 0.792, P < 0.01), but to be negatively correlated with prothrombin activity (r = - 0.511, P < 0.05) in patients with ACHBLF.

Conclusion: The TNF-alpha methylation patten is stable for the liver failure, suggesting the effect of environment on methylation.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • DNA Methylation
  • Female
  • Hepatitis B, Chronic / blood
  • Hepatitis B, Chronic / genetics*
  • Hepatitis B, Chronic / metabolism
  • Humans
  • Liver Failure, Acute / blood
  • Liver Failure, Acute / genetics
  • Liver Failure, Acute / metabolism
  • Male
  • Middle Aged
  • Promoter Regions, Genetic*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics*
  • Young Adult

Substances

  • Tumor Necrosis Factor-alpha