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This study aimed at evaluating the neuropharmacological impacts of betaine, a natural compound known for its antioxidant properties, in a rat model of Parkinson’s disease induced by rotenone.
Male Wistar rats were separated into various groups and administered betaine at two different doses (10 mg/kg and 20 mg/kg orally), in addition to rotenone (2 mg/kg subcutaneously), for 35 days.
Various parameters were analyzed to determine the effectiveness of betaine. After receiving rotenone, the subjects displayed various behavioral alterations such as catalepsy, delayed beam walk, postural instability, unusual movement patterns, reduced weight, altered rearing behavior, impaired muscle coordination, decreased locomotor activity, and weakened grip strength. Interestingly, these effects were notably alleviated when betaine was given alongside. Betaine demonstrated a reduction in rotenone-induced oxidative stress by lowering levels of thiobarbituric acid reactive substances (TBARS) and superoxide anion generation (SAG), while increasing levels of catalase (CAT) and glutathione (GSH) in the cerebrum and midbrain regions. Moreover, betaine helped alleviate the reduction in dopamine (DA) levels caused by rotenone-induced neurodegeneration. In general, the protective impact of betaine against rotenone-induced PD symptoms outperformed the typical treatment with Levodopa+Carbidopa (L+C), especially at the higher dosage of 20 mg/kg.
These results indicate that betaine shows potential as a therapeutic option for PD because of its antioxidant properties.
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