The overexpression of Thioredoxin-1 suppressing inflammation induced by methamphetamine in spleen

Drug Alcohol Depend. 2016 Feb 1:159:66-71. doi: 10.1016/j.drugalcdep.2015.11.021. Epub 2015 Nov 23.

Abstract

Background: Methamphetamine (METH) is an addictive psychostimulant and has been shown to induce oxidative stress and inflammation in various tissues. Thioredoxin-1 (Trx-1) plays the roles in regulating redox and inhibiting inflammation. Whether Trx-1 is involved in METH-induced inflammation is still unknown.

Methods: The present study was designed to investigate inflammatory factors in spleen of wild type and Trx-1 overexpression transgenic mice after METH treatment.

Results: We found the mRNA level of Trx-1 was decreased and mRNA level of Trx-1 binding protein-2 (TBP-2) was increased. The mRNA levels of tumor necrosis factor-α (TNF-α), interferon-γ(IFN-γ), interleukin-2 (IL-2), T-bet and signal transducer and activators of transcription 4 (STAT 4) were increased and the mRNA levels of IL-10, GA-TA-binding protein-3 (GATA-3) and STAT 6 were decreased. Overexpression of Trx-1 reversed the above effects induced by METH.

Conclusion: The present study showed for the first time that Trx-1 overexpression suppressed the inflammation induced by METH.

Keywords: Inflammatory mediators; Methamphetamine; Thioredoxin-1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carrier Proteins / biosynthesis
  • Central Nervous System Stimulants / adverse effects
  • GATA3 Transcription Factor / biosynthesis
  • Inflammation / chemically induced*
  • Inflammation / genetics
  • Inflammation / metabolism*
  • Interferon-gamma / biosynthesis
  • Interleukin-10 / biosynthesis
  • Interleukin-2 / biosynthesis
  • Methamphetamine / adverse effects*
  • Mice
  • Mice, Transgenic
  • STAT Transcription Factors / biosynthesis
  • Spleen / drug effects
  • Spleen / metabolism*
  • T-Box Domain Proteins / biosynthesis
  • T-bet Transcription Factor
  • Thioredoxins / biosynthesis
  • Thioredoxins / genetics*
  • Thioredoxins / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Carrier Proteins
  • Central Nervous System Stimulants
  • GATA3 Transcription Factor
  • Gata3 protein, mouse
  • Interleukin-2
  • STAT Transcription Factors
  • T-Box Domain Proteins
  • T-bet Transcription Factor
  • Tumor Necrosis Factor-alpha
  • Txnip protein, mouse
  • Interleukin-10
  • Methamphetamine
  • Thioredoxins
  • Interferon-gamma