AIM:To study the anti-inflammatory effects ofcholecystokinin-octapeptide(CCK-8)onlipopolysaccharide(LPS)-induced endotoxic shock(ES)and further investigate its signal transduction pathwaysinvolving p38 mitogen-activated protein kinase(MAPK)and IκB-α.METHODS:Eighty-four rats were divided randomly intofour groups:LPS(8 mg·kg~(-1),iv)induced ES;CCK-8(40 μg·kg~(-1),iv)pretreatment 10 min before LPS(8mg·kg~(-1));CCK-8(40 μg·kg~(-1),iv)or normal saline(control)groups.The inflammatory changes of lung andspleen,phagocytic function of alveolar macrophage,quantification of inflammatory cells in bronchoalveolarlavage(BAL)were investigated in rats by usinghematoxylin and eosin(HE)staining,phagocytosis ofCandida albicans and differential cell counting.Nitricoxide(NO)production in serum,lung and spleen wasmeasured with the Griess reaction.The mechanisminvolving p38 MAPK and IκB-α signal pathways wasinvestigated by Western blot.RESULTS:Inflammatory changes of lung and spleeninduced by LPS were alleviated by CCK-8,the increaseof NO induced by LPS in serum,lung and spleen wassignificantly inhibited and the neutrophil infiltration inBAL was significantly reduced by CCK-8.The numberof neutrophils was(52±10)×10~6 cells·L~(-1)in LPS group,while it decreased to(18±4)×10~6 cells·L~(-1)in CCK-8+LPS(P<0.01).The phagocytic rate of CCK-8 groupincreased to(62.49±9.49)%,compared with controlgroup(48.16±14.20)%,P<0.05.The phagocytosisrate was(85.14±4.64)% in LPS group,which reducedto(59.33±3.14)% in CCK-8+LPS group(P<0.01).Theresults of phagocytosis indexes showed similar changes.CCK-8 may play an important role in increasing theexpression of p38 MAPK and decreasing the degradationof IκB-α in lung and spleen of ES rats.CONCLUSION:CCK-8 can result in anti-inflammatory effects,which may be related to activation of p38 MAPKand inhibition on the degradation of IκB-α. AIM: To study the anti-inflammatory effects ofcholecystokinin-octapeptide (CCK-8) onlipopolysaccharide (LPS) -induced endotoxic shock (ES) and further investigate its signal transduction pathwaysinvolving p38 mitogen- activated protein kinase (MAPK) and IκB-α.METHODS (8 μg · kg -1, iv) induced ES; CCK-8 (40 μg · kg -1) iv iv) pretreatment for 10 min before LPS (8 mg · kg -1) 8 mg · kg -1); CCK-8 (40 μg · kg -1) iv) or normal saline (control) groups. Inflammatory factor of lung and complex, phagocytic function of alveolar macrophage, quantification of inflammatory cells in bronchoalveolar vessel (BAL) were investigated in rats by using hematoxylin and eosin (HE) staining, phagocytosis ofCandida albicans and differential cell counting. Nitricoxide (NO) production in serum, lung and spleen wasmeasured with the Griess reaction.The mechanisminvolving p38 MAPK and IKB -α signal pathways was investigated by Western blot .RESULTS: Inflammatory changes of lung and spleeninduced by LPS w The increase of NO induced by LPS in serum, lung and spleen wassignificantly inhibited and the neutrophil infiltration in BAL was significantly reduced by CCK-8. The number of neutrophils was (52 ± 10) × 10 ~ 6 cells · L (-1) in LPS group, while it decreased to (18 ± 4) × 10 ~ 6 cells · L -1 in CCK-8 + LPS (P <0.01) .The phagocytic rate of CCK-8 groupincreased (62.49 ± 9.49)%, compared with controlgroup (48.16 ± 14.20)%, P <0.05.The phagocytosis was (85.14 ± 4.64)% in LPS group, which reducedto (59.33 ± 3.14)% in CCK-8 + LPS group (P <0.01). The results of phagocytosis indexes showed similar changes. CCK-8 may play an important role in increasing theexpression of p38 MAPK and decreasing the degradationof IκB-α in lung and spleen of ES rats.CONCLUSION: CCK-8 can result in anti-inflammatory effects, which may be related to activation of p38 MAPK and inhibition on the degradation of IκB-α.