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Updated: Feb 12, 2026

Isolation and Characterization of Neutrophil-derived Microparticles for Functional Studies
Published on: March 2, 2018
Effect of methamphetamine exposure on the plasma levels of endothelial-derived microparticles
Azadeh Nazari1, Maryam Zahmatkesh2, Esmaeil Mortaz3
1Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Background:
Methamphetamine (Meth), a neurotoxin, induces inflammation, oxidative stress, and triggers endothelial dysfunction and cardiovascular disease which is the second cause of death among individuals with Meth-use disorder. Oxidative stress and inflammation trigger the microparticle (MP) release. These are extracellular vesicles extracted from cell surface and identified in biological fluids. MP levels alter during pathological conditions, suggesting its potential biomarker role. In this respect, we designed the present experiment to investigate the effects of Meth on the plasma level of the endothelial-derived microparticle (EMP).
Methods:
Animals received Meth (4 mg/kg i.p.) for 1, 7 and 14 days and then, the plasma level of EMPs was evaluated, using cell surface markers, including AnnexinV, CD144, CD31, CD41a antigens with the flow cytometry method. The biochemical indices and locomotor activity were also assessed in a rat model.
Results:
Meth increased locomotor activity (Meth-1, 277.12 ± 20.17; Meth-7, 262.25 ± 11.95; Meth-14, 265.75 ± 14.75), inflammatory and oxidative indices as evidenced by rising of the C-reactive protein (Meth-7, 39.4 ± 1.24; Meth-14, 38.58 ± 2.19, vs 8.65 ± 0.45, mg/L) and malondialdehyde (Meth-7, 9.74 ± 1.38; Meth-14, 14.6 ± 1.45, vs 4.43 ± 0.32 nmol/L) plasma levels. We also found that Meth triggered endothelial injury, as demonstrated by elevated levels of EMP (Meth-7, 4.77 ± 0.22; Meth-14, 5.91 ± 0.34, % total events/mL) compared with control group.
Conclusion:
Our data showed that Meth exposure stimulates inflammatory and oxidative pathways and facilitates the EMPs shedding. Measuring the level of EMPs might be applied as a potential diagnostic index to monitor the endothelial dysfunction in substance-use disorders.
Insights
Methamphetamine (Meth) exposure increases inflammation and oxidative stress, leading to endothelial injury. Measuring endothelial-derived microparticles (EMPs) may help monitor endothelial dysfunction in substance use disorders.
Area of Science:
- Toxicology
- Cardiovascular Disease
- Biomarkers
Background:
- Methamphetamine (Meth) is a neurotoxin linked to cardiovascular disease, the second leading cause of death in individuals with Meth-use disorder.
- Meth-induced inflammation and oxidative stress contribute to endothelial dysfunction.
- Microparticles (MPs), particularly endothelial-derived microparticles (EMPs), are released during pathological conditions and may serve as biomarkers.
Purpose of the Study:
- To investigate the impact of Methamphetamine on plasma levels of endothelial-derived microparticles (EMPs).
- To assess Methamphetamine's effects on inflammatory and oxidative stress markers.
- To evaluate changes in locomotor activity in a rat model.
Main Methods:
- Rats received Methamphetamine (4 mg/kg i.p.) for 1, 7, or 14 days.
- Plasma EMP levels were quantified using flow cytometry with specific cell surface markers (AnnexinV, CD144, CD31, CD41a).
- Biochemical indices (C-reactive protein, malondialdehyde) and locomotor activity were measured.
Main Results:
- Methamphetamine significantly increased locomotor activity across all treatment durations.
- Elevated levels of inflammatory (C-reactive protein) and oxidative stress (malondialdehyde) markers were observed.
- Plasma EMP levels were significantly higher in Methamphetamine-exposed rats, indicating endothelial injury.
Conclusions:
- Methamphetamine exposure activates inflammatory and oxidative stress pathways, promoting EMP release.
- Elevated EMP levels suggest significant endothelial dysfunction.
- Quantifying EMPs could serve as a potential diagnostic tool for monitoring endothelial damage in substance-use disorders.
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