目的观察脂多糖(LPS)攻击小鼠白细胞介素-4(IL-4)、IL-10的动态变化规律,以及八肽胆囊收缩素(CCK-8)对其表达的影响。方法随机将小鼠分组,每组7只。腹腔注射LPS10mg/kg,于攻击后0、2、4、6和12h检测血清、肺组织IL-4和IL-6表达高峰的时间。对照组腹腔注射生理盐水0.2ml;LPS组腹腔注射LPS10mg/kg;LPS+CCK-8组在注射LPS前30min腹腔注射CCK-8 60μg/kg;CCK-8组腹腔注射CCK-8 60μg/kg。用酶联免疫吸附法(ELISA)及逆转录-聚合酶链反应(PT—PCR)方法检测各组小鼠血清和肺组织中IL-4、IL-10的含量及其mRNA的表达情况。结果LPS攻击后2h血清及肺组织IL-4、IL-6均显著升高,血清IL-4、IL-6于4h和6h达高峰;肺组织IL-4、IL-6则均于6h达高峰。说明LPS攻击可使小鼠血清及肺组织中IL-4、IL-10的蛋白及mRNA表达均增加;预先注入CCK-8可使IL-4和IL-10的蛋白以及mRNA表达均进一步增加(P均〈O.01);而单独注射CCK-8对血清、肺组织IL-4、IL-10的表达无明显影响。结论CCK-8可能通过进一步增加LPS攻击小鼠IL-4、IL-10的表达参与抗炎反应过程,从而减轻LPS引起的肺组织炎症反应。
Objective To observe the effects of cholecystokinin octapeptide (CCK - 8) on the expression of anti -inflammatory cytokines interleukin - 4 (IL - 4) and IL - 10 in lipopolysaccharide (LPS) challenged mice. Methods Kunming mice were randomly assigned into four groups (each n = 7): ①Intraperitioneal injection of LPS (10 mg/kg), and the times of peak level of IL - 4 and IL - 6 expression in serum and lung tissue were noted at 0, 2, 4, 6 and 12 hours after challenge. ② Control group (intraperitioneal injection of normal saline 0.2 ml). ③LPS+CCK -8 group (intraperitioneal injection of CCK-8 60 μg/kg 30 minutes before giving LPS). ④CCK - 8 group (intraperitioneal injection injection CCK- 8 60 μg/kg) at different time points. The expressions of IL - 4 and IL - 10 in the serum and lung tissues were assayed by enzyme linked immunoadsorbent assay (ELISA) and reverse transcription - polymerase chain reaction (RT-PCR). Results Two hours after LPS challenge, IL - 4 and IL - 6 were increased significantly in serum and lung tissue. At 4 hours and 6 hours, serum IL - 4 and IL - 6 reached their peak levels, while in lung tissue they reached their peak levels at 6 hours. Pre - treatment of CCK - 8 augmented IL - 4 and IL - 10 expressions in LPS challenged mice (both P~0.01). But single CCK - 8 injection showed no significant effect on IL - 4 and IL - 10 in serum and lung tissue. Conclusion CCK - 8 is involved in the anti -inflammatory response by increasing the expressions of IL - 4, IL - 10 in LPS challenged mice, and in turn it alleviates the inflammatory response in lung tissue.