Wild grape alleviates nasal symptoms.
Islam, Rezwanul Tokushima University
Shaha, Aurpita Tokushima University
Nishida, Kohei Tokushima University
Yabumoto, Masami Medical Corporation Kinshukai
Ikeda, Hisashi Nab co., ltd.
Fujino, Hiromichi Tokushima University Tokushima University Educator and Researcher Directory
Kitamura, Yoshiaki Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Fukui, Hiroyuki Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
histamine H1 receptor
nuclear factor of activated T-cells
protein kinase Cδ
As expression level of allergic disease-sensitive genes are correlated with allergic symptom severity, suppression of these gene expressions could be good therapeutics. We have demonstrated that PKCδ signaling and NFAT signaling, involve in histamine H1 receptor (H1R) and IL-9 gene expressions, respectively, are responsible for the pathogenesis of allergic rhinitis. We explore anti-allergic compounds that suppress these signaling pathways and found that wild grape (WG) contains such compounds. Here, we investigated the effect of WG hot water extract (WGE) on the signaling pathways for PKCδ-mediated H1R and NFAT-mediated IL-9 gene expressions. WGE suppressed histamine/PMA-induced H1R gene up-regulation in HeLa cells. Toluene-2,4-diisocyanate (TDI)-induced H1R mRNA elevation in TDI-sensitized rats was also suppressed by WGE treatment. Treatment with WGE in combination with Awa-tea, suppresses NFAT signaling-mediated IL-9 gene, markedly alleviated nasal symptoms. Furthermore, WGE suppressed PMA-induced IL-33 gene up-regulation in Swiss 3T3 cells. Data suggest that combination of WGE, suppresses PKCδ signaling with Awa-tea, suppresses NFAT signaling would have distinct clinical and therapeutic advantages as a substitute for anti-allergic drugs. In addition, as the expression level of IL-33 mRNA was correlated with the blood eosinophils number in patients with pollinosis, WG could alleviate eosinophilic inflammation through the suppression of IL-33 gene expression.
The Journal of Medical Investigation
Faculty of Medicine Tokushima University
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