Baicalein attenuates methamphetamine-induced loss of dopamine transporter in mouse striatum

Ping Ho Wu, Yuh Chiang Shen, Yea Hwey Wang, Chin Wen Chi, Jiin Cherng Yen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

Abstract

Methamphetamine (METH) has been shown to cause dopaminergic neurotoxicity. By using the loss of dopamine transporter (DAT) as a marker of neurotoxicity, this study was aimed to investigate the neuroprotective effect of baicalein against METH-induced striatal damages in mice. Results from Western blotting showed that repeated METH administration (5 mg/kg, i.p., four injections at 2-h interval) caused 40% decrease of DAT level in mouse striatum measured at 72 h after the last injection. Despite of the ineffectiveness at high dose (3.0 mg/kg, i.p.), pretreatment with lower doses of baicalein (0.3-1.0 mg/kg, i.p.) significantly attenuated the METH-induced striatal DAT loss in a dose-dependent manner. Furthermore, baicalein diminished METH-induced increase in striatal malondialdehyde content and myeloperoxidase activity, markers for lipid peroxidation and neutrophil increase, respectively. In addition, the present study also revealed that baicalein effectively diminished the ROS production by leukocytes stimulated with METH or PMA, a phorbol ester used as a positive control of stimulant. Surprisingly, we found that METH-induced nNOS overexpression was further increased by the pretreatment with baicalein while the level of nNOS was not altered significantly by baicalein treatment alone. These results suggested that baicalein may attenuate methamphetamine-induced DAT loss by inhibiting the neutrophil increase and the lipid peroxidation caused by neutrophil-derived reactive oxygen species in striatum.

Original languageEnglish
Pages (from-to)238-245
Number of pages8
JournalToxicology
Volume226
Issue number2-3
DOIs
StatePublished - 21 Sep 2006

Keywords

  • Baicalein
  • Lipid peroxidation
  • Methamphetamine
  • Myeloperoxidase
  • Neuroprotection

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