AIM:To study the effect of cholecystokinin-octapeptide(CCK-8)on lipopolysaccharide(LPS)-induced pulmonaryartery smooth muscle cell(PASMCs)injury and the role ofheme oxygenase-1(HO-1),and to explore the regulationmechanism of c-Jun N-terminal kinase(JNK)and activatorprotein-1(AP-1)signal transduction pathway in inducingHO-1 expression further.METHODS:Cultured PASMCs were randomly divided into4 or 6 groups:normal culture group,LPS(10 mg/L),CCK-8(10~(-6) mol/L)plus LPS(10 mg/L)group,CCK-8(10~(-6) mol/L)group,zinc protoporphyrin 9(ZnPPIX)(10~(-6) mol/L)plus LPS(10mg/L)group,CCK-8(10~(-6) mol/L)plus ZnPPIX and LPS(10mg/L) group.Seven hours after LPS administration,ulterstructrual changes and content of malondialdehyde(MDA)of PASMCs in each group were investigated byelectron microscopy and biochemical assay respectively.HO-1 mRNA and protein of PASMCs in the former4 groupswere examined by reverse transcriptase polymerase chainreaction(RT-PCR)and immunocytochemistry staining.Changes of c-los expression and activation of JNK ofPASICs in the former 4 groups were detected withimmunocytochemistry staining and Western blot 30minafter LPS administration.RESULTS:The injuries of PASMCs and the increases ofMDA content induced by LPS were alleviated and significantlyreduced by CCK-8(P<0.05).The specific HO-1 inhibitor-ZnPPIX could worsen LPS-induced injuries and weakenthe protective effect of CCK-8.The expressions of c-fos,p-JNK protein and HO-1 mRNA and protein were all slightlyincreased in LPS group,and significantly enhanced byCCK-8 further(P<0.05).CONCLUSION:HO-1 may be a key factor in CCK-8attenuated injuries of PASMCs induced by LPS,and HO-1expression may be related to the activation of JNK andactivator protein(AP-1). AIM: To study the effect of cholecystokinin-octapeptide (CCK-8) on lipopolysaccharide (LPS) -induced pulmonary artery smooth muscle cell (PASMCs) injury and the role of heme oxygenase-1 (HO- 1), and to explore the regulation mechanism of c (JNK) and activatorprotein-1 (AP-1) signal transduction pathway in inducing HO-1 expression further.METHODS: Cultured PASMCs were randomly divided into 4 or 6 groups: normal culture group, LPS (10 mg / L (10 mg / L) and CCK-8 (10 -6 mol / L) plus LPS (10 mg / L) (10 mg / L) plus ZnPPIX and LPS (10 mg / L) plus CCK-8 (10 -6 mol / L) plus LPS administration (10 mg / L) changes and content of malondialdehyde (MDA) of PASMCs in each group were investigated by electron microscopy and biochemical assay respectively. HO-1 mRNA and protein of PASMCs in the former 4 groups were examined by reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry staining. Change of c-los expression and activation of JNK of PASICs in the former 4 groups were detected with immunocytochemistry staining and Western blot 30 min after LPS administration .RESULTS: The injuries of PASMCs and the increases of MDA content induced by LPS were significantly reduced and significantly reduced by CCK-8 (P <0.05). The specifics of c-fos, p-JNK protein and HO-1 mRNA and protein were all slightly increased in LPS group, and significantly increased in LPS-induced injuries and weakenthe protective effect of CCK- enhanced by CCK-8 further (P <0.05). CONCLUSION: HO-1 may be a key factor in CCK-8 attenuated injuries of PASMCs induced by LPS, and HO- 1 expression may be related to the activation of JNK and activator protein ).