Sho-seiryu-to Suppresses Histamine Signaling at the Transcriptional Level in TDI-Sensitized Nasal Allergy Model Rats

• Published in: Allergology international Vol. 58; no. 1; pp. 81 - 88
• Main Authors: Das, Asish Kumar, Mizuguchi, Hiroyuki, Kodama, Madoka, Dev, Shrabanti, Umehara, Hayato, Kitamura, Yoshiaki, Matsushita, Chiyo, Takeda, Noriaki, Fukui, Hiroyuki
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 2009; Elsevier
• Subjects: allergy; Animals; Cytokines - genetics; Disease Models, Animal; Drugs, Chinese Herbal - pharmacology; Drugs, Chinese Herbal - therapeutic use; gene expression; Histamine - physiology; histamine H1 receptors; histamine signaling; histidine decarboxylase; Histidine Decarboxylase - genetics; Hypersensitivity - drug therapy; Male; Medicine, Kampo; Nasal Mucosa - drug effects; Rats; Rats, Inbred BN; Receptors, Histamine H1 - genetics; RNA, Messenger - analysis; Signal Transduction - drug effects; Th2 cytokines; Toluene 2,4-Diisocyanate - pharmacology; allergy; Th2 cytokines; histamine H1 receptors; histidine decarboxylase; gene expression; histamine signaling
• ISSN: 1323-8930; 1440-1592
• DOI: 10.2332/allergolint.O-07-526

The therapeutic use of Kampo medicine, Sho-seiryu-to (SST) in allergic disorders is well known. As histamine plays a central role in allergic diseases, it is possible that SST affects the allergy-related histamine signaling. In this study, we investigated the effect of SST on allergy-related histamine signaling in the nasal mucosa of toluene 2, 4-diisocyanate (TDI)-sensitized nasal allergy model rats. Six-week-old male, Brown Norway rats were sensitized for 2 weeks with 10 μl of 10% TDI, and after a 1 week interval, provocation was initiated with the same amount of TDI. SST (0.6 g/rat) was given orally 1 hour before TDI treatment began for a period of 3 weeks. Nasal symptoms were scored for 10 minutes immediately after TDI-provocation. The genes expression in nasal mucosa was determined using real-time quantitative RT-PCR. SST significantly suppressed TDI-induced nasal allergy-like symptoms. TDI provocation showed a significant up-regulation of histamine H1 receptor (H1R) and histidine decarboxylase (HDC) gene expressions. Prolonged pre-treatment of SST significantly suppressed the mRNA levels of H1R and HDC that was up-regulated by TDI. SST also suppressed TDI-induced interleukin (IL)-4 and IL-5 mRNA elevation. However, SST showed no significant effect for TDI-induced mRNA elevation of IL-13. These results demonstrate that SST alleviates nasal symptoms by the inhibition of histamine signaling through suppression of TDI-induced H1R and HDC gene up-regulation. SST also suppresses cytokine signaling through suppression of IL-4 and IL-5 gene expression. Suppression of histamine signaling may be a novel mechanism of SST in preventing allergic diseases.