【摘要】 目的探讨八肽胆囊收缩素(cholecystokinin octapeptide,CCK-8)对脂多糖(lipopo- lysaccharide,LPS)诱导急性肺损伤(acute lung injury,ALI)小鼠炎症反应的影响。方法复制LPS致ALI小鼠模型。实验动物随机分为生理盐水对照组、LPS组(腹腔注射LPS)、LPS+CCK-8组(注射LPS前30 min腹腔注射CCK-8)及CCK-8组(单独注射CCK-8)。用酶联免疫吸附法(ELISA)及逆转录-聚合酶链反应(PT-PCR)检测不同时间点各组小鼠血清、肺组织中白细胞介素-1β(IL-1β)、IL-6的含量及mRNA表达情况。观察各组肺组织光镜病理改变。结果腹腔注射LPS可成功复制ALI小鼠模型,肺组织病理显示,在LPS组12h时可见肺间质充血、水肿,大量炎性症细胞浸润,腹腔预注射CCK-8可明显改善肺组织病理变化;腹腔注射LPS可使小鼠血清及肺组织中IL-1β、IL-6表达增加,分别于注射后2h及4h达到高峰,预先注入CCK-8可显著抑制IL-1β、IL-6的表达。结论CCK-8可能通过抑制ALI小鼠IL-1β、IL-6的表达参与抗炎反应过程,从而减轻LPS诱导的ALI小鼠肺组织炎症反应。更多还原

【Abstract】 Objective To investigate the effect of Cholecystokinin octapeptide(CCK-8)on mice with acute lung injury(ALI)induced by lipopolysaccharide(LPS).Methods ALI murine model were duplicated by injection of LPS intraperitoneally.Mice were randomly divided into saline control group,LPS group(injection of LPS intraperitoneally),LPS+CCK-8 group(injection of CCK-8 30 rain before LPS)and CCK-8 group(injection of CCK-8).The expressions of interleukin-1β(IL- 1β)and IL-6 in serum and lung tissues were detected by ELISA and RT-PCR.Lung pathological changes were also observed in each group.Results ALI murine model were successfully duplicated by in- jection of LPS intraperitoneally.Histologically,massive alveolar interstitial tissue edema,hemorrhage, and inflammatory cell infiltration were observed at 12 h of LPS group,and they could be alleviated in LPS+CCK-8 group.The expressions of IL-1β,IL-6 increased markedly in serum and lung of LPS- attacked mice,and reached peak at the time of 2,4 h after injection of LPS respectively.Pre-treatment of CCK-8 decreased both IL-1βand IL-6 expressions.Conclusions CCK-8 involved in the anti- inflammatory response by inhibiting the expressions of IL-1β,IL-6 in LPS-attacked mice,which could alleviate the inflammatory response in lung tissue on mice with ALI.更多还原