A Study of The Relation Between Mitochondrial Syntaxin-17, Oxidative Stress and Inflammation Through Targeting mTOR Pathway in Induced Parkinsonism in Experimental Rats

Background: Parkinsonism is a chronic neurodegenerative disorder that is distinguished by impaired motor function. It is caused by the degeneration of dopaminergic neurones in the substantia nigra and a deficiency of dopamine in the brain. The aim of this study was to determine relationship between the mitochondrial Syntaxin-17, oxidative-stress and inflammation via the mammalian target of rapamycin (mTOR) pathway in induced parkinsonism in a rat model of rotenone-induced parkinsonism. Aims: This experimental study was designed to shed light on investigating the relationship between mitochondrial Syntaxin-17, oxidative stress, and inflammation via the mammalian target of rapamycin in experimentally induced parkinsonism in rats. Materials and Methods: 40 male albino rats were employed for the test, while being allocated randomly to two equal groups as follows: Control group (group I), rotenone-administered group (group II). Total antioxidant capacity tissue homogenate level was measured using spectrophotometric assay. Syntaxin-17 tissue homogenate and mammalian target of rapamycin (mTOR) tissue homogenate levels were measured by Enzyme-linked immunosorbent assay. Results: Syntaxin-17, mammalian target of rapamycin and total antioxidant capacity levels in rotenone-administered group were significantly decreased than control group. Conclusion: There is a significant relationship between Syntaxin-17, mammalian target of rapamycin (mTOR) and oxidative stress.