| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2009478 | Pesticide Biochemistry and Physiology | 2012 | 7 Pages |
Damage to the mitochondrial electron transport chain by rotenone has been suggested to be an important factor in the pathogenesis of many neurodegenerative disorders. Adult male Wister albino rats were orally treated with Portulaca oleracea (purslane) at a dose of 1.5 mL/kg body weight for 12 days. Pre-treatment, post-treatment and co-treatment of rotenone (12 mg/kg body weight) was given orally. The striatum level of Na+/K+-ATPase activity, glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD) were evaluated. Protein carbonyl and hydrogen peroxide (H2O2) levels were also determined. Results revealed that purslane administration induced a marked improvement in all the parameters that were studied. Purslane reversed the increases in protein carbonyl and H2O2 that were a consequence of the oxidative stress generated by rotenone administration. Additionally, RT-PCR results showed that whilst GPx transcription was decreased due to rotenone administration, it was up-regulated with purslane treatment. In conclusion, the present study provided a clear evidence that purslane possesses promising activity against rotenone-induced neurodegeneration. Thus, it may be useful against neurotoxicity induced by environmental neurotoxins.
Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideHighlights► We examine role of purslane on rotenone model for Parkinson’s disease. ► Neurotoxin induced neurodegeneration. ► Oxidative stress in Parkinson’s disease. ► Purslane as a potential therapeutic value for neurodegenerative diseases.
