چکیده مقاله
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 200–250 g were used and randomly divided into target groups The 2×106 bone marrow stem cells were injected from tail vein for Mesenchymal stem cell group other group received intraperitoneal caffeic acid phenethyl ester 10μM granulocyte colony stimulating factor 75 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 < 0 05 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 5 38 ± 0 24 and caffeic acid phenethyl ester 6 2±0 1 GSH Px amount in granulocyte colony stimulating factor 4 69 ± 0 11 , Mesenchymal stem cell 4 14 ± 0 08 and caffeic acid phenethyl ester 0 20±0 01 was closer to the control group Activity of SOD was increased in granulocyte colony stimulating factor 14 26 ± 3 11 , Mesenchymal stem cell 11 35 ± 2 11 , and caffeic acid phenethyl ester FRAP level significantly increased in the granulocyte colony stimulating factor administration 1 13 ± 0 1 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
کلیدواژهها
نویسندگان
Mitra Yousefpour
Department of physiology, Aja University of medical sciences, Tehran, Iran
Manouchehr Safari
Department of anatomy, Semnan University of medical sciences, Tehran, Iran
Laya Ghahari
Department of anatomy, Aja University of medical sciences, Tehran, Iran
شیوه ارجاع
Yousefpour, Mitra and Safari, Manouchehr and Ghahari, Laya,1400,Mutual interaction of oxidative stress and Parkinson disease: Antioxidant role,Second National Conference on Psychopathological Studies and New Treatments,Tehran
ارائهشده در
مجموعه مقالات دومین کنفرانس ملی مطالعات آسیب شناسی روانی و روش های نوین درمان14 بهمن 1400 · تهران