首页> 外文期刊>Journal of Ethnopharmacology: An Interdisciplinary Journal Devoted to Bioscientific Research on Indigenous Drugs >Neuroprotective effect of SuHeXiang Wan in Drosophila models of Alzheimer's disease.
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Neuroprotective effect of SuHeXiang Wan in Drosophila models of Alzheimer's disease.

机译:苏和香丸对果蝇阿尔茨海默氏病模型的神经保护作用。

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AIM OF THE STUDY: SuHeXiang Wan (SHXW) is a Chinese traditional medicinal prescription that consists of 15 crude herbs. SHXW has been used to treat central nervous depression, seizures, infantile convulsion and stroke, and its essential oil has been shown to have anticonvulsant and antioxidative activity. The goal of this study was to investigate the beneficial effects of SHXW on the neurological phenotypes of Drosophila AD models. MATERIALS AND METHODS: We evaluated the effects of a modified SHXW (called KSOP1009) intake on the AD-like phenotypes of Drosophila AD models, which express human Abeta42 in their developing eyes or neurons. RESULTS: When the flies were kept on the media containing 5 mug/ml of KSOP1009 extract, Abeta42-induced eye degeneration, apoptosis, and the locomotive dysfunctions were strongly suppressed. However, Abeta42 fibril deposits in the Abeta42 overexpressing model were not affected by treatment with KSOP1009 extract. Conversely, KSOP1009 extract intake significantly suppressed the constitutive active form of hemipterous, a JNK activator, while it induced eye degeneration and JNK activation, which has been recognized as an important mediator of Abeta42-associated neuro-cytotoxicity. CONCLUSIONS: In conclusion, the results of this study suggest that KSOP1009 confers a therapeutic potential to AD-like pathology of Abeta42 overexpressing Drosophila model via suppression of the hyperactivation of JNK activity and apoptosis.
机译:研究目的:苏合香丸(SHXW)是一种中药传统处方,由15种粗制草药组成。 SHXW已被用于治疗中枢神经抑制,癫痫发作,婴儿惊厥和中风,其精油已被证明具有抗惊厥和抗氧化活性。这项研究的目的是调查SHXW对果蝇AD模型的神经表型的有益影响。材料和方法:我们评估了改良的SHXW(称为KSOP1009)摄入量对果蝇AD模型的AD样表型的影响,果蝇AD模型在发育中的眼睛或神经元中表达人Abeta42。结果:将果蝇保持在含有5杯/毫升KSOP1009提取物的培养基上时,Abeta42诱导的眼部退化,细胞凋亡和机车功能障碍被强烈抑制。但是,Abeta42过表达模型中的Abeta42原纤维沉积不受KSOP1009提取物处理的影响。相反,KSOP1009提取物的摄入显着抑制了JNK激活剂半指的组成型活性形式,同时它诱导了眼部变性和JNK激活,JNK激活被认为是Abeta42相关的神经细胞毒性的重要介体。结论:总之,这项研究的结果表明,KSOP1009通过抑制JNK活性的过度激活和凋亡,为过表达果蝇Abeta42模型的AD样病理赋予了治疗潜力。

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