
Anti‐inflammatory effect of amurensin H on asthma‐like reaction induced by allergen in sensitized mice 1
Author(s) -
LI Yitang,
YAO Chunsuo,
BAI Jinye,
LIN Mao,
CHENG Guifang
Publication year - 2006
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2006.00330.x
Subject(s) - ovalbumin , bronchoalveolar lavage , eosinophil , mucus , immunology , eosinophilia , cytokine , medicine , tumor necrosis factor alpha , interleukin 5 , interleukin , lung , inflammation , asthma , biology , antigen , ecology
Aim: To explore the anti‐inflammatory effects of amurensin H on asthma‐like reaction induced by allergen in sensitized mice. Methods: BALB/c mice were sensitized by ovalbumin (OVA, ip) on d 0 and d 14 and challenged with 1 % OVA on d 18 to 22. Mice developed airway eosinophilia, mucus hypersecretion, and elevation in cytokine levels. Mice were administered amurensin H orally at the doses of 49, 70, or 100 mg/kg once every day from d 15 to the last day. Bronchoalveolar lavage fluid (BALF) were collected at 24 h and 48 h after the last OVA challenge. Levels of tumor necrosis factor‐α (TNF‐α), interleukin 4 (IL‐4), interleukin 5 (IL‐5), and interleukin 13 (IL‐13) in BALF were measured using ELISA method. Differential cell counts of macrophages, lymphocytes, neutrophils and eosinophils were performed in 200 cells per slide (one slide per animal). Lung tissue sections of 6‐um thickness were stained with Mayer's hematoxylin and eosin for assessment of cell infiltration, mucus production, and tissue damage. Results: Oral administration of amurensin H significantly inhibited OVA‐induced increases in total cell counts, eosinophil counts, and TNF‐α, IL‐4, IL‐5 and IL‐13 levels in BALF. In addition, amuresin H dramatically decreased OVA‐induced lung tissue damage and mucus production. Conclusion: Amurensin H may have therapeutic potential for the treatment of allergic airway inflammation.