Acta Pharmacologica Sinica 2006 June; 27 (6): 735-740; doi: 10.1111/j.1745-7254.2006.00330.x

 
Original Article
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Anti-inflammatory effect of amurensin H on asthma-like reaction induced by allergen in sensitized mice1
 

Yi-tang LI2, Chun-suo YAO3, Jin-ye BAI2, Mao LIN3, Gui-fang CHENG2,4

2Department of Pharmacology, Institute of Materia Medica, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100050, China; 3Department of Photochemistry, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China

 

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-µm 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.

 

Keywords: amurensin H; asthma; ovalbumin; tumor necrosis factor-α; Th2 cells; cytokines

 
1 Project supported by grants from the Insti-tute of Materia Medica, Peking Union Medical College and Chinese Academy of Medical Sciences (No 231766).

4 Correspondence to Prof Gui-fang CHENG.
Phn 86-10-6316-5192.
Fax 86-10-6301-7757.
E-mail chenggf@imm.ac.cn
Received 2005-12-14     Accepted 2006-01-27

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