Inhibitory effects of cryptoporus polysaccharide on airway constriction, eosinophil release, and chemotaxis in guinea pigs
Abstract
AIM:
To study effects of cryptoporus polysaccharide (CP) on antigen-induced bronchoconstriction, eosinophil peroxidase (EPO) release in vivo, and on platelet activating factor (PAF)-induced eosinophil chemotaxis in vitro in guinea pig.
METHODS:
The asthma model of guinea pig was formed with ovalbumin (OVA). The changes of lung resistance (R(L)) and dynamic lung compliance (C(dyn)), EPO level in bronchoalveolar lavage fluids (BALF) and eosinophil migration were determined.
RESULTS:
Pretreatment of CP at doses of 3, 9, and 27 mg/kg by intragastric gavage (i.g.), qd for 10 d, inhibited early asthma response in a dose-dependent manner. Inhibitory rates of mean increase value from 1 to 30 min of R(L) were 34.8 %, 74.4 % (P<0.05), and 79.6 % (P<0.05), respectively. Inhibitory rate of mean reduction value of C(dyn) were 22.9 %, 40.5 % (P<0.01), and 66.5 % (P<0.01), respectively. Pretreatment of CP at doses of 3, 9, and 27 mg/kg also inhibited late asthma response, and the reduction of EPO level in BALF were 3.1 %, 16.9 % (P<0.01), and 20.1 % (P<0.01), respectively. The inhibitory rates of CP at concentrations of 0.13, 1.3, 13, 130 nmol/L to eosinophil migration induced by PAF were 6.8 %, 17.2 % (P<0.05), 29.6 % (P<0.01), and 35.9 % (P<0.01).
CONCLUSION:
CP protects lung against increase of R(L) and reduction of C(dyn), decreases EPO level in the asthma model, and inhibits eosinophil chemotaxis induced by PAF. The results suggest that CP may be a novel antiinflammatory agent for the treatment of asthma and allergic diseases.
Keywords:
To study effects of cryptoporus polysaccharide (CP) on antigen-induced bronchoconstriction, eosinophil peroxidase (EPO) release in vivo, and on platelet activating factor (PAF)-induced eosinophil chemotaxis in vitro in guinea pig.
METHODS:
The asthma model of guinea pig was formed with ovalbumin (OVA). The changes of lung resistance (R(L)) and dynamic lung compliance (C(dyn)), EPO level in bronchoalveolar lavage fluids (BALF) and eosinophil migration were determined.
RESULTS:
Pretreatment of CP at doses of 3, 9, and 27 mg/kg by intragastric gavage (i.g.), qd for 10 d, inhibited early asthma response in a dose-dependent manner. Inhibitory rates of mean increase value from 1 to 30 min of R(L) were 34.8 %, 74.4 % (P<0.05), and 79.6 % (P<0.05), respectively. Inhibitory rate of mean reduction value of C(dyn) were 22.9 %, 40.5 % (P<0.01), and 66.5 % (P<0.01), respectively. Pretreatment of CP at doses of 3, 9, and 27 mg/kg also inhibited late asthma response, and the reduction of EPO level in BALF were 3.1 %, 16.9 % (P<0.01), and 20.1 % (P<0.01), respectively. The inhibitory rates of CP at concentrations of 0.13, 1.3, 13, 130 nmol/L to eosinophil migration induced by PAF were 6.8 %, 17.2 % (P<0.05), 29.6 % (P<0.01), and 35.9 % (P<0.01).
CONCLUSION:
CP protects lung against increase of R(L) and reduction of C(dyn), decreases EPO level in the asthma model, and inhibits eosinophil chemotaxis induced by PAF. The results suggest that CP may be a novel antiinflammatory agent for the treatment of asthma and allergic diseases.