2017 Fiscal Year Final Research Report
Molecular mechanism of steroids for the suppression of histamine H1 receptor signaling.
Project/Area Number |
15K07933
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Biological pharmacy
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Research Institution | Osaka Ohtani University (2017) The University of Tokushima (2015-2016) |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | ヒスタミンH1受容体遺伝子発現シグナル / ステロイドシグナル / PKCδ / Hsp90 |
Outline of Final Research Achievements |
The expression level of an allergic disease-sensitive gene is correlated with the symptoms severity. We demonstrated that histamine H1 receptor (H1R) gene is a pollinosis-sensitive gene. Maackiain was isolated as an anti-allergic compound that suppresses H1R signaling, and Hsp90 was identified as its intracellular target molecule that was common to the steroid signaling. We examined the effect of steroids on the H1R signaling. We also investigated the effect of maackiain on the steroid signaling. Suppression of H1R signaling by steroids was ambiguous compared to the results from the animal experiments. Maackain increased steroid-stimulated up-regulation of anti-inflammatory gene expression. These data suggest that steroids might suppress H1R signaling indirectly through the histamine-cytokine network. Data also suggest that maackiain show the anti-allergic effect through not only the suppression of H1R signaling but also reinforcement the anti-inflammatory effect of steroids.
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Free Research Field |
分子薬理学
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