Objective:To investigate effect of cordycepin on lung injury in rats with acute respiratory distress syndrome(ARDS)and its mechanism.Methods:Sixty Wistar rats were randomly divided into control group,lipopolysaccharide group(LPS),cordyce-pin low-dose group(5 mg/kg),cordycepin medium-dose group(15 mg/kg),cordycepin high-dose group(30 mg/kg),Compound C group(high-dose cordycepin 30 mg/kg+AMPK inhibitor 15 mg/kg),with 10 rats in each group.ARDS model of LPS rats was estab-lished,pathological changes of lung tissues were observed by HE staining and lung tissue pathological injury score was performed;wet/dry weight ratio(W/D)of rat lungs was measured;activity of myeloperoxidase(MPO)was detected;IL-6,IL-1β and TNF-α were measured by ELISA;malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH)were detected by kit;Western blot was used to detect expressions of AMP-activated protein kinase(AMPK),p-AMPK,mammalian target of rapamy-cin(mTOR),p-mTOR,P70 ribosomal protein S6 kinase(p70S6K)and p-p70S6K.Results:Compared with control group,rats in LPS group had obvious lung tissue damage,and a large number of inflammatory cells infiltration,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were increased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expres-sions were increased(P<0.05),SOD,GSH levels were decreased,p-AMPK/AMPK protein expression was decreased(P<0.05);after treatment with cordycepin,lung tissue damage was reduced,a small amount of inflammatory cells were infiltrated,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were decreased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expressions were decreased(P<0.05),SOD,GSH levels were increased,p-AMPK/AMPK protein expressions were increased(P<0.05);AMPK inhibitor Compound C reversed improvement of cordycepin on lung injury in ARDS rats.Conclusion:Cordycepin can improve LPS induced lung injury of rats,reduce inflammatory and oxidative stress,whose mechanism may be related to regulation of AMPK/mTOR/p70S6K pathway.

Objective:To investigate effect of cordycepin on lung injury in rats with acute respiratory distress syndrome(ARDS)and its mechanism.Methods:Sixty Wistar rats were randomly divided into control group,lipopolysaccharide group(LPS),cordyce-pin low-dose group(5 mg/kg),cordycepin medium-dose group(15 mg/kg),cordycepin high-dose group(30 mg/kg),Compound C group(high-dose cordycepin 30 mg/kg+AMPK inhibitor 15 mg/kg),with 10 rats in each group.ARDS model of LPS rats was estab-lished,pathological changes of lung tissues were observed by HE staining and lung tissue pathological injury score was performed;wet/dry weight ratio(W/D)of rat lungs was measured;activity of myeloperoxidase(MPO)was detected;IL-6,IL-1β and TNF-α were measured by ELISA;malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH)were detected by kit;Western blot was used to detect expressions of AMP-activated protein kinase(AMPK),p-AMPK,mammalian target of rapamy-cin(mTOR),p-mTOR,P70 ribosomal protein S6 kinase(p70S6K)and p-p70S6K.Results:Compared with control group,rats in LPS group had obvious lung tissue damage,and a large number of inflammatory cells infiltration,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were increased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expres-sions were increased(P<0.05),SOD,GSH levels were decreased,p-AMPK/AMPK protein expression was decreased(P<0.05);after treatment with cordycepin,lung tissue damage was reduced,a small amount of inflammatory cells were infiltrated,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were decreased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expressions were decreased(P<0.05),SOD,GSH levels were increased,p-AMPK/AMPK protein expressions were increased(P<0.05);AMPK inhibitor Compound C reversed improvement of cordycepin on lung injury in ARDS rats.Conclusion:Cordycepin can improve LPS induced lung injury of rats,reduce inflammatory and oxidative stress,whose mechanism may be related to regulation of AMPK/mTOR/p70S6K pathway.