Abstract:

OBJECTIVE: To study the protective effect and mechanisms of ethyl pyruvate(EP) on pulmonary inflammation induced by chlorine gas. METHODS：Adult male SD rats were exposed to chlorine gas of 2 536 mg/m3 or normal air for 20 min in a whole-body dynamic exposure chamber. EP (40 mg/kg) or vehicle(saline) was given by intraperitoneal injections immediately after chlorine gas exposure. Rats were killed at 6 hours and 24 hours after chlorine gas exposure. At 6 hours，levels of TNF-α，IL-1β and IL-8 in bronchoalveolar lavage fluid (BALF) and the nuclear translocation of nuclear factor κB (NF-κB) in the lung were evaluated. At 24 hours，the expression of HMGB1 and the activity of type-ⅡA secretary phospholipase A2 (sPLA2-ⅡA)were measured. RESULTS：At 6 hours after chlorine gas exposure，levels of TNF-α，IL-1β and IL-8 in BALF as well as NF-κB nuclear translocation increased significantly(P<0.05). Furthermore，at 24 hours，HMGB1 expression and sPLA2-ⅡA activity too were significantly increased(P<0.05). EP treatment attenuated these changes(P<0.05). CONCLUSION： Chlorine gas induced inflammation in the lung via activation of inflammatory mediators at early as well as late stage. EP treatment attenuated inflammation in the lung induced by chlorine gas.

Key words: chlorine gas, inflammation, ethyl pyruvate, lung tissue