Pyrrolidine dithiocarbamate ameliorates rotenone-induced Parkinson’s disease in rats
| Autor: | Noha F. Abdelkader, Amina S. Attia, Nadia M. S. Arafa, Dalaal M. Abdallah, Afaf A. Ain-Shoka |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
lcsh:RS1-441 Pharmacology medicine.disease_cause Neuroprotection lcsh:Pharmacy and materia medica 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Pyrrolidine dithiocarbamate Rotenone TBARS medicine Inflammation biology Glutamate receptor Glutathione 030104 developmental biology chemistry Biochemistry Oxidative stress Myeloperoxidase Parkinson’s disease biology.protein 030217 neurology & neurosurgery |
| Zdroj: | Bulletin of Faculty of Pharmacy, Cairo University, Vol 55, Iss 1, Pp 107-113 (2017) |
| ISSN: | 1110-0931 |
| DOI: | 10.1016/j.bfopcu.2016.11.003 |
| Popis: | Pyrrolidine dithiocarbamate (PDTC), a low-molecular-weight thiol antioxidant, possesses neuroprotection; however, its possible modulatory effect in Parkinson’s disease (PD) has not been tested. Male Wistar rats were injected with rotenone to induce PD-like symptoms. Histopathological findings showed that striatal neurons were degenerated following rotenone administration, an effect that was accompanied by behavioral deficits. Furthermore, rotenone decreased striatal dopamine (DA) and glutamate and prominently increased serotonin, GABA, glutathione (GSH), thiobarbituric acid reactive substances (TBARS), and myeloperoxidase (MPO) levels. Daily treatment with PDTC protected against rotenone induced changes at the microscopic level, decreased the extent of motor dysfunctions, and markedly increased DA and suppressed glutamate levels. It also reduced TBARS, GSH, and MPO. Whereas, rotenone neither affected striatal caspase-3 activity nor tumor necrosis factor-α level, PDTC treatment reduced the later. The current study reveals the effectiveness of PDTC against rotenone-induced PD via enhancement of DA, as well as antioxidant and anti-inflammatory properties. |
| Databáze: | OpenAIRE |
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