Mutual interaction of oxidative stress and Parkinson disease: Antioxidant role

Oxidative stress is induced by an imbalanced redox state or dysfunction of the antioxidant system. oxidative stress plays a central role in a common pathophysiology of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Parkinson’s disease is a common neurodegenerative disease mainly involved in the progressive loss of dopaminergic neurons. In this study, the relationship between Parkinson's disease and the effect of oxidative stress was investigated. We conducted a series of studies on Parkinson's that examined the effect of oxidative stress on it, as well as the protective effect of antioxidants on it. The effect of antioxidants such as caffeic acid phenethyl ester, granulocyte colony-stimulating factor and Mesenchymal stem cell was investigated. Adult male Wistar rats (weighing ۲۰۰–۲۵۰ g) were used and randomly divided into target groups. The ۲×۱۰۶ bone marrow stem cells were injected from tail vein for Mesenchymal stem cell group . other group received intraperitoneal caffeic acid phenethyl ester (۱۰μM). granulocyte colony-stimulating factor (۷۵ μg/kg) were used after induced PD. The rat brains were removed and processed for immunohistochemical studies. For assessing stress oxidative markers such as MDA, SOD, GSH-Px, and FRAP, the bilateral midbrain immediately was isolated from the brain stems. All data were expressed as mean ± SD. Data were analyzed by one-way ANOVA, followed by Tukey's post hoc test for dopaminergic neuron counts. value of p < ۰.۰۵ was considered to be statistically significant. The results of oxidative stress tests showed changes in antioxidant enzymes after the administration of Mesenchymal stem cell, granulocyte colony-stimulating factor, and caffeic acid phenethyl ester. MDA levels significantly decreased following the administration of granulocyte colony-stimulating factor ( ۵.۳۸ ± ۰.۲۴ )and caffeic acid phenethyl ester (۶.۲±۰.۱). GSH-Px amount in granulocyte colony-stimulating factor (۴.۶۹ ± ۰.۱۱), Mesenchymal stem cell (۴.۱۴ ± ۰.۰۸) and caffeic acid phenethyl ester (۰.۲۰±۰.۰۱) was closer to the control group. Activity of SOD was increased in granulocyte colony-stimulating factor (۱۴.۲۶ ± ۳.۱۱ ), Mesenchymal stem cell (۱۱.۳۵ ± ۲.۱۱), and caffeic acid phenethyl ester. FRAP level significantly increased in the granulocyte colony-stimulating factor administration(۱.۱۳ ± ۰.۱) and other treatment groups. Increased MDA and decreased SOD and GSH-Px cause mitochondrial and then neuronal destruction. These events could eventually participate in PD pathogenesis. The decreased activity of these enzymes is indirectly responsible for neuronal loss and probably has an essential role in the onset of PD. The balance of these enzymes will protect nerve cells. In our studies, results showed that Antioxidant that used in study can protect neurons against MPTP toxin that cause by Parkinson diseases. This neuroprotection is due to the strong antioxidant properties. Oxidative stress plays a role in the pathogenesis of Parkinson's disease. However, our data provide evidence that antioxidants have neuroprotective effects in PD rats. Its anti-oxidative capacity to scavenge free radicals and resulted in the survival of dopamine neurons.

Keywords:

Oxidative stress , parkinson , antioxidant , rat