摘要：

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)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 μ g @ kg-1, iv) or normal saline(control) groups.The inflammatory changes of lung andspleen, phagocytic function of alveolar macrophage,quantification of inflammatory calls 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 mechanisminvestigated 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)× 106 cells. L-1 in LPS group,while it decreased to (18±4)×106 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 degradation of IκB-αin Iung and spleen of ES rats.CONCLUSION: CCK-8 can result in anti-inflammatoryeffects, which may be related to activation of p38 MAPK and inhibition on the degradation of IκB-α.

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