[Gene expressions of LTC4 synthase homologs in Con A-induced mouse hepatitis and regulative effect of cyclosporine A]

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2007 May;36(3):241-6. doi: 10.3785/j.issn.1008-9292.2007.03.006.
[Article in Chinese]

Abstract

Objective: To explore the gene expressions of LTC4 synthase homologs in concanavalin A (Con A)-induced mouse hepatitis and regulation role of cyclosporine A (Cs A) treatment.

Methods: Male Balb/c mouse liver injury model was developed by iv injection of Con A (20 mg/kg) and protected by Cs A pretreatment (150 mg/kg) before Con A administration. Blood samples were collected at indicated times after Con A treatment with or without Cs A pretreatment. Liver damage was assessed by serum transaminase ALT and AST measurement and histological evaluation. Meantime, three LTC4 synthase homolog gene expressions were determined by RT-PCR.

Results: Serum ALT and AST upregulation were accompanied with histological damage at 2 h after Con A administration, and further aggravated at 8 h. mGST2 gene expression increased 1.7 fold at 2 h and 1.9 fold at 8 h, while the expression of LTC4 S and mGST3 changed little. Pretreatment with Cs A prevented mouse liver from injury by Con A and partly inhibited the mGST2 gene expression upregulation.

Conclusions: Administration of Con A in mouse lead to a significant increase of mGST2 gene expression without any significant effect on LTC4 S and mGST3 mRNA levels. Cs A pretreatment results in protection of liver damage, whereas fails to fully inhibit the increase of mGST2 gene expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Aspartate Aminotransferases / blood
  • Chemical and Drug Induced Liver Injury / enzymology
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Concanavalin A / administration & dosage
  • Concanavalin A / toxicity*
  • Cyclosporine / pharmacology*
  • Gene Expression Regulation, Enzymologic / genetics
  • Glutathione Transferase / genetics*
  • Hepatitis, Animal / chemically induced
  • Hepatitis, Animal / enzymology
  • Hepatitis, Animal / prevention & control*
  • Immunosuppressive Agents / pharmacology
  • Injections, Intravenous
  • Isoenzymes / genetics
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Immunosuppressive Agents
  • Isoenzymes
  • Concanavalin A
  • Cyclosporine
  • Glutathione Transferase
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • leukotriene-C4 synthase