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María Eugenia Jaramillo-Flores,Herry Heriyati Permady,Ana Maria Puebla-Pérez,Eduardo Padilla,Eugenia del Carmen Lugo-Cervantes,Jorge Ivan Delgado-Saucedo,Eva Ramón-Gallegos 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.5
Ditaxis heterantha seeds are used as spices for flavoring and coloring food. Two new apocarotenoids derived from the seeds, heteranthin and ditaxin, were evaluated for their in vitro cytotoxic effects in murine lymphoma cells lines. Bioabsorption in mice and preventive and antitumor effects of the apocarotenoids were determined. Ditaxin and heteranthin showed cytotoxic effects in vitro against murine malignant cells and normal splenocyte cells. The 50% inhibitory concentration (IC_50) for ditaxin in splenocytes was 0.1825 mM; in L5178Y, the IC_50 was 0.1923 mM. The heteranthin IC_50 in splenocytes was 0.1325 mM; in L5178Y, the value was 0.3889 mM. The maximum ditaxin plasma concentration was found after 2 hours of administration (mean±standard deviation, 7.5±2.05 μg/mL). Oral administration of the D. heterantha extract (100 mg/kg per day) for 14 days after the L5178Y lymphoma cell implantation showed no significant effect compared with groups that were not pretreated. However, tumor inhibition in groups treated intraperitoneally before inoculation with the L5178Y cells showed a significant difference (P<.001) compared with the groups not pretreated.
RAS–MAPK–MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1
Park, Jeehye,Al-Ramahi, Ismael,Tan, Qiumin,Mollema, Nissa,Diaz-Garcia, Javier R.,Gallego-Flores, Tatiana,Lu, Hsiang-Chih,Lagalwar, Sarita,Duvick, Lisa,Kang, Hyojin,Lee, Yoontae,Jafar-Nejad, Paymaan,Sa Nature Publishing Group, a division of Macmillan P 2013 Nature Vol.498 No.7454
Many neurodegenerative disorders, such as Alzheimer’s, Parkinson’s and polyglutamine diseases, share a common pathogenic mechanism: the abnormal accumulation of disease-causing proteins, due to either the mutant protein’s resistance to degradation or overexpression of the wild-type protein. We have developed a strategy to identify therapeutic entry points for such neurodegenerative disorders by screening for genetic networks that influence the levels of disease-driving proteins. We applied this approach, which integrates parallel cell-based and Drosophila genetic screens, to spinocerebellar ataxia type 1 (SCA1), a disease caused by expansion of a polyglutamine tract in ataxin 1 (ATXN1). Our approach revealed that downregulation of several components of the RAS–MAPK–MSK1 pathway decreases ATXN1 levels and suppresses neurodegeneration in Drosophila and mice. Importantly, pharmacological inhibitors of components of this pathway also decrease ATXN1 levels, suggesting that these components represent new therapeutic targets in mitigating SCA1. Collectively, these data reveal new therapeutic entry points for SCA1 and provide a proof-of-principle for tackling other classes of intractable neurodegenerative diseases.