Neuroscience letters · 2022
Post treatment with Gastrodin suppresses oxidative stress and attenuates motor disorders following 6-OHDA induced Parkinson disease.
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Sadeghian Zohre, Eyvari-Brooshghalan Shahla, Sabahi Mohammadmahdi, Nourouzi Nahal, Haddadi Rasool
Аннотация
BACKGROUND & OBJECTIVE: Researchers are currently trying to find new therapies with better symptomatic activity and fewer side effects to manage Parkinson's disease (PD). Although the protective effect of pre-treatment by Gastrodin (Gst) on a PD model has been evaluated, in the current experimental study, we investigated the symptomatic therapeutic effects of Gst microinjection in the same PD model but in the post-parkinsonism induction condition.
METHODS: Parkinsonism was induced by unilateral infusion of 6- hydroxydopamine (6-OHDA; 8 μg/ 2 μl/ rat) into the central region of the substantia nigra pars compacta (SNc). After the recovery period and confirmation of parkinsonism, daily Gst treatment in three doses (20, 40, 80 µg/ 2 µ/ rat, continued for ten days with motor monitoring by bar test and rotarod examinations. Moreover, lipid peroxidation and myeloperoxidase activity were evaluated.
RESULTS: In this model of 6-OHDA-induced parkinsonism, Gst treatment in all three doses showed a dose dependent symptomatic improvement in motor imbalance (P < 0.001) catalepsy (P < 0.001), decreased lipid peroxidation (P < 0.001) and SNc myeloperoxidase activity (P < 0.001).
CONCLUSIONS: 6-OHDA induced parkinsonism symptomatically improved behaviorally with Gst post-induction treatment along with decreased markers of oxidative stress and microglial activation. We suggest that this agent is a candidate for symptomatic treatment of human PD.
METHODS: Parkinsonism was induced by unilateral infusion of 6- hydroxydopamine (6-OHDA; 8 μg/ 2 μl/ rat) into the central region of the substantia nigra pars compacta (SNc). After the recovery period and confirmation of parkinsonism, daily Gst treatment in three doses (20, 40, 80 µg/ 2 µ/ rat, continued for ten days with motor monitoring by bar test and rotarod examinations. Moreover, lipid peroxidation and myeloperoxidase activity were evaluated.
RESULTS: In this model of 6-OHDA-induced parkinsonism, Gst treatment in all three doses showed a dose dependent symptomatic improvement in motor imbalance (P < 0.001) catalepsy (P < 0.001), decreased lipid peroxidation (P < 0.001) and SNc myeloperoxidase activity (P < 0.001).
CONCLUSIONS: 6-OHDA induced parkinsonism symptomatically improved behaviorally with Gst post-induction treatment along with decreased markers of oxidative stress and microglial activation. We suggest that this agent is a candidate for symptomatic treatment of human PD.