Objective To explore the effect and mechanism of artemisinin on the lung injury caused by cardiac arrest and cardiopulmonary resuscitation(CPR).Methods Twenty-two white pigs were randomly divided into three groups of S(sham operation,6 pigs),C(underwent CPR,8 pigs)and T(underwent CPR+artemisinin,8 pigs).The CPR models were established in groups of C and T using electrical stimulation-induced cardiac arrest for 9 minutes and artificial CPR for 6 minutes.Artemisinin 4.8 mg/kg was infused intravenously within 2 hours after CPR modeling successfully in group T.Groups of S and C were infused the same amount of normal saline.The extravascular lung water index(ELWI)and pulmonary vascular permeability index(PVPI)were measured by pulse indicator continous cardiac output monitor at the time points of before(T0)and 1(T1),2(T2)and 4 hours(T3)after modeling.At 24 hours after modeling,the protein expressions of NOD-like receptor pyrin domain 3(NLRP3),cleaved Caspase-1 and gasdermin D-N terminal(GSDMD-N)were detected by Western blot,and IL-1β and IL-18 contents were detected by ELISA.Results Compared with group S,ELWI and PVPI in group C were increased at T1-T3,and PVPI in group T was increased at T1 and T2(P＜0.05).Compared with group C,ELWI and PVPI in group T were decreased at T2 and T3(P＜0.05).Compared with group S,the protein expressions of cleaved Caspase-1 and GSDMD-N,and the contents of IL-1β and IL-18 in groups of C and T were increased(P＜0.05).Compared with group C,the protein expressions of NLRP3,cleaved Caspase-1 and GSDMD-N,and the contents of IL-1β and IL-18 in group T were decreased(P＜0.05).Conclusion Artemisinin can reduce the lung injury caused by cardiac arrest and CPR by inhibiting NLRP3 inflammasome-mediated pyroptosis in pig lung tissues.
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