[Protective effect of N-acetyl-L-cysteine on liver and lung injury in mice after partial hepatic ischemia/reperfusion]

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2007 Jul;19(7):394-7.
[Article in Chinese]

Abstract

Objective: To investigate the changes in Toll-like receptor 2/4(TLR2/4) gene expression in liver and lung in ischemia/reperfusion (I/R) injury with or without preconditioning of N-acetyl-L-cysteine (NAC).

Methods: BALB/c mice were used in a model of partial hepatic I/R injury and randomly divided into sham-injury control group (SH group), hepatic I/R group and hepatic I/R with NAC pretreatment group (NAC group), each n=10. The level of tumor necrosis factor-alpha (TNF-alpha) in portal vein and plasma alanine aminotransferase (ALT) were measured at 1 hour and 3 hours respectively after reperfusion, the expressions of TLR2/4 mRNA and protein in liver and lung were observed with reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting at the same time points.

Results: Compared with I/R group, the expressions of TLR2/4 mRNA and protein in liver and lung in NAC group were decreased at same time points (P<0.05 or P<0.01). The level of TNF-alpha in portal vein and plasma ALT increased continually in I/R group at 1 hour and 3 hours after reperfusion compared with SH group, however, they were significantly lowered in the group pretreated by NAC (P<0.05 or P<0.01).

Conclusion: TLR2/4 is activated in liver and lung in the process of partial hepatic I/R injury. NAC can inhibit the activation of TLR2/4 and the induction of TNF-alpha resulted from I/R injury via modulating the state of redox process; thus it might mitigate liver and lung injury following partial hepatic I/R in mice.

Publication types

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

MeSH terms

  • Acetylcysteine / pharmacology*
  • Alanine Transaminase / blood
  • Animals
  • Antioxidants / pharmacology
  • Disease Models, Animal
  • Liver / blood supply*
  • Liver / metabolism
  • Lung / metabolism
  • Lung Injury / metabolism
  • Lung Injury / prevention & control*
  • Mice
  • Mice, Inbred BALB C
  • RNA, Messenger / genetics
  • Random Allocation
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / prevention & control*
  • Toll-Like Receptor 2 / genetics
  • Toll-Like Receptor 2 / metabolism
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antioxidants
  • RNA, Messenger
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Alanine Transaminase
  • Acetylcysteine