Albizia lebbeck suppresses histamine signaling by the inhibition of histamine H sub(1 receptor and histidine decarboxylase gene transcriptions)

Histamine plays major roles in allergic diseases and its action is mediated mainly by histamine H sub(1 receptor (H1R). We have demonstrated that histamine signaling-related H1R and histidine decarboxylase (HDC) genes are allergic diseases sensitive genes and their expression level affects severity...

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Published inInternational immunopharmacology Vol. 11; no. 11; pp. 1766 - 1772
Main Authors Nurul, Islam Mohammed, Mizuguchi, Hiroyuki, Shahriar, Masum, Venkatesh, Pichairajan, Maeyama, Kazutaka, Mukherjee, Pulok K, Hattori, Masashi, Choudhuri, Mohamed Sahabuddin Kabir, Takeda, Noriaki, Fukui, Hiroyuki
Format Journal Article
LanguageEnglish
Published 01.11.2011
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Summary:Histamine plays major roles in allergic diseases and its action is mediated mainly by histamine H sub(1 receptor (H1R). We have demonstrated that histamine signaling-related H1R and histidine decarboxylase (HDC) genes are allergic diseases sensitive genes and their expression level affects severity of the allergic symptoms. Therefore, compounds that suppress histamine signaling should be promising candidates as anti-allergic drugs. Here, we investigated the effect of the extract from the bark of Albizia lebbeck (AL), one of the ingredients of Ayruvedic medicines, on H1R and HDC gene expression using toluene-2,4-diisocyanate (TDI) sensitized allergy model rats and HeLa cells expressing endogenous H1R. Administration of the AL extract significantly decreased the numbers of sneezing and nasal rubbing. Pretreatment with the AL extract suppressed TDI-induced H1R and HDC mRNA elevations as well as [) super(3)H]mepyramine binding, HDC activity, and histamine content in the nasal mucosa. AL extract also suppressed TDI-induced up-regulation of IL-4, IL-5, and IL-13 mRNA. In HeLa cells, AL extract suppressed phorbol-12-myristate-13-acetate- or histamine-induced up-regulation of H1R mRNA. Our data suggest that AL alleviated nasal symptoms by inhibiting histamine signaling in TDI-sensitized rats through suppression of H1R and HDC gene transcriptions. Suppression of Th2-cytokine signaling by AL also suggests that it could affect the histamine-cytokine network.
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ISSN:1567-5769
DOI:10.1016/j.intimp.2011.07.003