Therapeutic Effects of S-Petasin on Disease Models of Asthma and Peritonitis.
10.4062/biomolther.2014.069
- Author:
Kyoung Pil LEE
1
;
Saeromi KANG
;
Min Soo NOH
;
Soo Jin PARK
;
Jung Min KIM
;
Hae Young CHUNG
;
Nam Kyung JE
;
Young Geun LEE
;
Young Whan CHOI
;
Dong Soon IM
Author Information
1. Molecular Inflammation Research Center for Aging Intervention (MRCA) and College of Pharmacy, Pusan National University, Busan 609-735, Republic of Korea. imds@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
S-petasin;
Anti-allergy;
Anti-inflammation;
COX-2;
Degranulation;
Mast Cell;
Macrophage
- MeSH:
Animals;
Asthma*;
Eosinophils;
Leukocytes, Mononuclear;
Lymphocytes;
Macrophages;
Macrophages, Peritoneal;
Mast Cells;
Mice;
Peritoneal Cavity;
Peritonitis*;
Petasites;
RNA
- From:Biomolecules & Therapeutics
2015;23(1):45-52
- CountryRepublic of Korea
- Language:English
-
Abstract:
To explore the anti-allergic and anti-inflammatory effects of extracts of Petasites genus, we studied the effects of s-petasin, a major sesquiterpene from Petasites formosanus (a butterbur species) on asthma and peritonitis models. In an ovalbumin-induced mouse asthma model, s-petasin significantly inhibited the accumulations of eosinophils, macrophages, and lymphocytes in bronchoalveolar fluids. S-petasin inhibited the antigen-induced degranulation of beta-hexosamidase but did not inhibit intracellular Ca2+ increase in RBL-2H3 mast cells. S-petasin inhibited the LPS induction of iNOS at the RNA and protein levels in mouse peritoneal macrophages. Furthermore, s-petasin inhibited the production of NO (the product of iNOS) in a concentration-dependent manner in the macrophages. Furthermore, in an LPS-induced mouse model of peritonitis, s-petasin significantly inhibited the accumulation of polymorpho nuclear and mononuclear leukocytes in peritoneal cavity. This study shows that s-petasin in Petasites genus has therapeutic effects on allergic and inflammatory diseases, such as, asthma and peritonitis through degranulation inhibition in mast cells, suppression of iNOS induction and production of NO in macrophages, and suppression of inflammatory cell accumulation.
