Abstract
It has been recognized that Gastrodia elata Bl (GE), an oriental herb medicine, ameliorates various neurological disorders, that GE modulates the monoaminergic and GABAergic systems, and that GE possess antioxidant activities. We examined whether GE affects methamphetamine (MA)-induced striatal dopaminergic toxicity in mice. Treatment with MA (7.5 mg/kg, i.p. × 4) resulted in significant decreases in behavioural activity (as shown by locomotor activity and rota rod performance), dopamine level, tyrosine hydroxylase (TH) activity, and TH protein expression (as evaluated by immunocytochemistry and western blot analysis). In addition, MA treatment showed significant increases in lipid peroxidation [as evaluated by 4-hydroxy-2-nonenal (4-HNE) expression and malondialdehyde formation], protein oxidation (as shown by protein carbonyl expression and its formation), and reactive oxygen species (ROS) formation. Treatment with GE significantly attenuates MA-induced behavioural and dopaminergic impairments, and oxidative stresses in a dose-dependent manner. Our results suggest that GE treatment shows anti-dopaminergic effects in response to MA insult via, at least in part, inhibiting oxidative stresses in the striatum of the mice.
Highlights
Gastrodia elata Bl (GE) is a well-known herb agent that has been used to treat headache, paralysis, migraine, and other neurological disorders in oriental countries for centuries [1]
Earlier evidences suggest that GE exerts antioxidant activities, which are attributable to its components, and that their antioxidant effect in vitro is more potent than that by melatonin [3]
We evaluated the effects of GE on the dopaminergic impairments and oxidative stresses [i.e., lipid peroxidation and protein oxidation, and reactive oxygen species (ROS)] induced by MA
Summary
Gastrodia elata Bl (GE) is a well-known herb agent that has been used to treat headache, paralysis, migraine, and other neurological disorders in oriental countries for centuries [1]. Prolonged GE treatment significantly increased dopamine (DA) concentration and decreased DA turnover in the striatum of the rats, suggesting that GE modulates DA system in the rats [2]. Earlier evidences suggest that GE exerts antioxidant activities, which are attributable to its components (i.e. hydroxybenzyl aclcohol, vanillyl alcohol, vanillin and hydroxybenzaldehyde), and that their antioxidant effect in vitro is more potent than that by melatonin [3]. MA-induced dopaminergic toxicity has been considered to be one of the important models for PD [5, 11, 12]. The present study was designed to investigate the pharmacological activity of GE on dopaminergic neurons to MA toxicity in mice. We evaluated the effects of GE on the dopaminergic impairments and oxidative stresses [i.e., lipid peroxidation and protein oxidation, and reactive oxygen species (ROS)] induced by MA
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