Related Experiment Video
Updated: Aug 6, 2026
A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
Published on: January 22, 2016
Baicalein attenuates methamphetamine-induced loss of dopamine transporter in mouse striatum
Ping-Ho Wu1, Yuh-Chiang Shen, Yea-Hwey Wang
1Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan, ROC.
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 72h 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.
Insights
Baicalein, a natural compound, shows neuroprotective effects against methamphetamine-induced neurotoxicity. It reduces dopamine transporter loss and oxidative stress in mice, suggesting therapeutic potential for methamphetamine-related brain damage.
Area of Science:
- Neuroscience
- Pharmacology
- Toxicology
Background:
- Methamphetamine (METH) causes significant dopaminergic neurotoxicity.
- Dopamine transporter (DAT) loss is a key marker for METH-induced neurotoxicity.
- Investigating neuroprotective agents is crucial for mitigating METH's adverse effects.
Purpose of the Study:
- To investigate the neuroprotective potential of baicalein against METH-induced striatal damage in mice.
- To assess baicalein's effect on DAT levels and oxidative stress markers following METH exposure.
Main Methods:
- Mice were administered METH and varying doses of baicalein.
- Western blotting was used to measure DAT levels in the striatum.
- Malondialdehyde content and myeloperoxidase activity were assessed as markers of oxidative stress and neutrophil infiltration.
Main Results:
- METH administration significantly decreased striatal DAT levels.
- Baicalein pretreatment dose-dependently attenuated METH-induced DAT loss.
- Baicalein reduced METH-induced increases in malondialdehyde and myeloperoxidase activity, and inhibited ROS production.
Conclusions:
- Baicalein exhibits neuroprotective effects against METH-induced striatal neurotoxicity.
- The protective mechanism involves inhibiting neutrophil-driven oxidative stress and lipid peroxidation.
- Baicalein may offer a therapeutic strategy for METH-induced neurotoxicity.
