Abstract
The present study aimed at evaluating the protective and therapeutic efficacy of omega-3 against motor impairment and brain biochemical disturbances in rotenone-induced mice model of Parkinson's disease (PD). Sixty animals were divided into six groups (10 each): mice of the 1 st group were used as controls, they were injected subcutaneously ( s c ) with the vehicle (50 µl dimethylsulfoxide (DEMSO) + 950 µl sunflower oil /kg body weight) every other day for 30 days; the 2 nd group, mice model of Parkinson’s disease (PD), were injected (s c ) with rotenone (3 mg/kg dissolved in vehicle every other day for 30 days ). the 3 rd group, mice were given rotenone for 30 days followed by a stopping (recovery) period of other 30 days to validate the persistency of the PD model; the 4 th group (protection group), mice received orally Omega-3 oil (300 mg/kg) daily an hour before every rotenone injection for 30 days; the 5 th and 6 th groups (therapeutic groups ), mice were treated orally with Omega-3 oil daily for 7 and 15 days respectively after the induction of PD mice model. Data obtained revealed an impairment of the motor activity in mice of PD model as indicated from the decreased time of the forelimb hanging test. This was associated with a state of oxidative stress in the brain of PD model as indicated from the increase in lipid peroxidation (increased malondialdehyed, MDA, level) and nitric oxide (NO), and the decrease in reduced glutathione (GSH). A significant decrease in the levels of dopamine, norepinephrine, serotonin, AChE activity and a significant increase in TNF-α level was recorded in the PD model. The present findings show that both the protection by or oral treatment with omega-3 for 15 days could ameliorate the rotenone- induced oxidative stress and inflammation in brain of PD mice model. In addition, omega-3 either as protection or treatment daily for 15 days was effective in restoring the decrease in dopamine and norepinephrine induced in the brain of PD mice model. In conclusion, the present study demonstrates that omega-3 supplementation potentially reverses the motor, and neurochemical alternations induced by rotenone in mice model of PD.
Highlights
Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease, with a male –to –female ratio of about 3:2 in most studies [1, 2]
When the mice model of PD were treated daily with omega-3 for 7 and 15 days, the decrease in forelimb hanging time induced by rotenone returned to non-significant change as compared to control value
Data illustrated in figures (2 and 3) show that rotenoneinduced mice model of PD was accompanied by significant increases in brain levels of lipid peroxidation (MDA) by 82.29% and nitric oxide (NO) by 60.82% respectively and a significant decrease in the level of GSH by 35.30% Figure (4) as all compared to their levels in control mice
Summary
Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease, with a male –to –female ratio of about 3:2 in most studies [1, 2]. Clinical Neurology and Neuroscience 2018; 2(1): 12-22 by self-perpetuating cascades involving a myriad of deleterious events at various stages including mitochondrial dysfunction, short-term and long-term oxidative and nitrosative stress, energy crisis, excitotoxicity, neuroinflammation and protein aggregation [7]. These events work together to promote cell death. Oxidative stress and mitochondrial dysfunction are responsible for the pathological features of PD, such as neuronal death and apoptosis [8, 9]
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