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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。
Objective To investigate the effect of cholecystokinin octapeptide (CCK-8) on the inflammatory reaction in lipopolysaccharide-induced acute lung injury (ALI) -induced mice. Methods LPS induced ALI mouse model. The experimental animals were randomly divided into saline control group, LPS group (intraperitoneal injection LPS), LPS + CCK-8 group (CCK-8 intraperitoneal injection 30 min before LPS injection) and CCK-8 group (CCK-8 injection alone). The levels of IL-1β, IL-6 in serum and lung tissue were detected by ELISA and PT-PCR at different time points Content and mRNA expression. The pathological changes of lung tissue were observed by light microscope. Results The model of ALI mice was successfully established by intraperitoneal injection of LPS. Pulmonary histopathology showed that pulmonary interstitial congestion, edema, infiltration of inflammatory cells and pretreatment with CCK-8 in the LPS group could significantly improve the pathological changes of lung tissue ; Intraperitoneal injection of LPS could increase the expression of IL-1β and IL-6 in serum and lung tissue of mice, reaching the peak at 2h and 4h after injection respectively. Pretreatment with CCK-8 significantly inhibited the expression of IL-1β and IL-6 . Conclusion CCK-8 may be involved in the process of anti-inflammatory reaction by inhibiting the expression of IL-1β and IL-6 in ALI mice, so as to reduce the lung inflammation induced by LPS in ALI mice.