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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >L-deprenyl protects against rotenone-induced, oxidative stress-mediated dopaminergic neurodegeneration in rats.
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L-deprenyl protects against rotenone-induced, oxidative stress-mediated dopaminergic neurodegeneration in rats.

机译：L-异戊二烯可防止鱼藤酮诱导的大鼠氧化应激介导的多巴胺能神经变性。

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摘要

The present study investigated oxidative damage and neuroprotective effect of the antiparkinsonian drug, L-deprenyl in neuronal death produced by intranigral infusion of a potent mitochondrial complex-I inhibitor, rotenone in rats. Unilateral stereotaxic intranigral infusion of rotenone caused significant decrease of striatal dopamine levels as measured employing HPLC-electrochemistry, and loss of tyrosine hydroxylase immunoreactivity in the perikarya of ipsilateral substantia nigra (SN) neurons and their terminals in the striatum. Rotenone-induced increases in the salicylate hydroxylation products, 2,3- and 2,5-dihydroxybenzoic acid indicators of hydroxyl radials in mitochondrial P2 fraction were dose-dependently attenuated by L-deprenyl. L-deprenyl (0.1-10mg/kg; i.p.) treatment dose-dependently attenuated rotenone-induced reductions in complex-I activity and glutathione (GSH) levels in the SN, tyrosine hydroxylase immunoreactivity in the striatum or SN as well as striatal dopamine. Amphetamine-induced stereotypic rotations in these rats were also significantly inhibited by deprenyl administration. The rotenone-induced elevated activities of cytosolic antioxidant enzymes superoxide dismutase and catalase showed further significant increase following L-deprenyl. Our findings suggest that unilateral intranigral infusion of rotenone reproduces neurochemical, neuropathological and behavioral features of PD in rats and L-deprenyl can rescue the dopaminergic neurons from rotenone-mediated neurodegeneration in them. These results not only establish oxidative stress as one of the major causative factors underlying dopaminergic neurodegeneration as observed in Parkinson's disease, but also support the view that deprenyl is a potent free radical scavenger and an antioxidant.
机译：本研究调查了抗帕金森病药物L-异戊二烯在大鼠鼻内输注有效线粒体复合物-I抑制剂鱼藤酮所致神经元死亡中的氧化损伤和神经保护作用。使用HPLC-电化学法测定，鱼藤酮的单侧立体定向鼻内输注导致纹状体多巴胺水平显着降低，并且同侧黑质（SN）神经元周围核及其纹状体末端的酪氨酸羟化酶免疫反应性丧失。肾上腺素诱导的水杨酸酯羟基化产物的增加，线粒体P2组分中羟基的2,3-和2,5-二羟基苯甲酸指示剂被L-异戊烯基剂量依赖性地减弱。 L-异戊二烯（0.1-10mg / kg;腹膜内）治疗剂量依赖性地减弱鱼藤酮诱导的SN中复合物I活性和谷胱甘肽（GSH）水平，纹状体或SN中酪氨酸羟化酶免疫反应性以及纹状体多巴胺的降低。在安非他明给药后，这些大鼠中苯丙胺诱导的定型旋转也被显着抑制。鱼藤酮诱导的胞质抗氧化酶超氧化物歧化酶和过氧化氢酶活性升高，继L-异戊二烯基之后进一步显着增加。我们的发现表明，单侧鼻内注射鱼藤酮可在大鼠中复制PD的神经化学，神经病理学和行为特征，而L-异戊二烯可以从鱼藤酮介导的神经变性中拯救多巴胺能神经元。这些结果不仅将氧化应激确立为在帕金森氏病中观察到的多巴胺能神经变性背后的主要病因之一，而且还支持了异戊二烯基是有效的自由基清除剂和抗氧化剂的观点。

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