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Journal Article
Research Support, Non-U.S. Gov't
Neuroprotective effect of SuHeXiang Wan in Drosophila models of Alzheimer's disease.
Journal of Ethnopharmacology 2011 April 13
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 Aβ42 in their developing eyes or neurons.
RESULTS: When the flies were kept on the media containing 5 μg/ml of KSOP1009 extract, Aβ42-induced eye degeneration, apoptosis, and the locomotive dysfunctions were strongly suppressed. However, Aβ42 fibril deposits in the Aβ42 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 Aβ42-associated neuro-cytotoxicity.
CONCLUSIONS: In conclusion, the results of this study suggest that KSOP1009 confers a therapeutic potential to AD-like pathology of Aβ42 overexpressing Drosophila model via suppression of the hyperactivation of JNK activity and apoptosis.
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 Aβ42 in their developing eyes or neurons.
RESULTS: When the flies were kept on the media containing 5 μg/ml of KSOP1009 extract, Aβ42-induced eye degeneration, apoptosis, and the locomotive dysfunctions were strongly suppressed. However, Aβ42 fibril deposits in the Aβ42 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 Aβ42-associated neuro-cytotoxicity.
CONCLUSIONS: In conclusion, the results of this study suggest that KSOP1009 confers a therapeutic potential to AD-like pathology of Aβ42 overexpressing Drosophila model via suppression of the hyperactivation of JNK activity and apoptosis.
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