Poster Topical Area: Nutritional Immunology

Location: Hall D

Poster Board Number: 837

P21-006 - Blockade of thrombin-induced lung inflammation and airway destruction by astragalin in a murine asthma model

Sunday, Jun 10
8:00 AM – 6:00 PM


Chronic obstructive pulmonary diseases such as chronic bronchitis and emphysema are progressive lung diseases characterized by irreversible airflow obstruction and chronic inflammation of the airways. Growing evidence supports that there is epidemiological association between different allergic diseases including asthma and venous thrombosis. Astragalin (kaempferol 3-O-glucoside) is a flavonoid present in persimmon leaves and green tea seeds, and exhibits antioxidant and anti-inflammatory activity. This study elucidated that astragalin inhibited thrombin-induced lung inflammation to injury in bronchial cells, lung alveolar epithelial cells and ovalbumin (OVA)-challenged mice.


A549 cells were treated with 1-20 μM astragalin and continuously stimulated with 10 U/ml thrombin for up to 24 h. BALB/c mice were sensitized with OVA by a subcutaneous injection twice on day 0 and day 14. For the dietary interventions, 10 or 20 mg/kg BW astragalin solution was administrated via oral gavage to OVA-sensitized mice. On the day 28, 29 and 30, 5% OVA inhalation to mice was performed for 20 min in a plastic chamber linked to an ultrasonic nebulizer.


Non-toxic astragalin at 1-20 μM attenuated the induction of protease activated receptor-2 (PAR-2) known as coagulation factor II (thrombin) receptor-like-1, in 10 U/ml thrombin-exposed alveolar epithelial cells. It was found that oral supplementation of 10-20 mg/kg astragalin suppressed the induction of CD11b and F4/80 with inhibition of small airway destruction in OVA-exposed mouse airways and lungs. In addition, the PAR-2 induction was highly elevated in bronchial airways of asthmatic lungs. These results demonstrated that astragalin inhibited the OVA exposure-induced airway inflammation and injury deteriorated by thrombosis.


Platelet aggregation and its subsequent microvascular thrombosis could exacerbate asthmatic lung injury. Thus, inhibition of thrombosis by astragalin can be a potential target for alleviating asthma exacerbation.


Yun-Ho Kim

Chuncheon-si, Kangwon-do, Republic of Korea