α7亚单位的N型乙酰胆碱受体对急性呼吸窘迫综合征小鼠CD11b和炎症因子的影响  

Effects ofα7nAChR on CD11b and inflammatory cytokines in mice with acute respiratory distress syndrome

作　　者：孙琼 余燕梅[1] 刘凡 殷宗宝[1] SUN Qiong;YU Yanmei;LIU Fan;YIN Zongbao(Department of Emergency,Haikou People's Hospital,Haikou,Hannan 570208,China)

机构地区：[1]海口市人民医院急诊科,海南海口570208

出　　处：《中国热带医学》2024年第1期82-86,101,共6页China Tropical Medicine

基　　金：海南省自然科学基金项目(No.821RC759)。

摘　　要：目的探讨α7亚单位的N型乙酰胆碱受体(nicotinic acetylcholine receptorsα7,α7nAChR)对急性呼吸窘迫综合征(acute respiratory distresssyndrome,ARDS)小鼠CD11b、白细胞介素-1β(interleukin-1 beta,IL-1β)、白细胞介素-18(interleukin-18,IL-18)、肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)的影响。方法健康清洁级雄性Balb/C小鼠40只(6周),完全数字随机分为正常组(N组)、生理盐水对照组(NS组)、ARDS组(A组)、ARDS+段离颈部两侧迷走神经给予乙酰胆碱受体激动剂组(J组),每组各10只正常饲养。用HE染色观察各组小鼠右肺结构,检测肺组织湿重/体质量比值(LWW/DW比值),采用流式细胞仪检测小鼠肺泡灌洗液CD11b的百分比,采用实时荧光定量聚合酶链反应(RT-qPCR)法检测左肺组织IL-1βmRNA、IL-18 mRNA和TNF-αmRNA的表达,酶联免疫吸附试验(enzyme linked immunosorbent assay,ELISA)双抗体夹心法测定各组小鼠血清IL-18含量。结果N组和NS组小鼠右肺HE染色显示结构正常,而A组小鼠肺间质有大量的炎性细胞浸润,肺泡壁增厚、肺泡结构破坏明显,肺泡腔融合。J组小鼠肺泡结构较完整、有少许破损、肺泡腔存在。A组小鼠肺泡灌洗液CD11b百分比高于其他3组,分别与N组、NS组、J组比较差异有统计学意义(P<0.05)。J组小鼠左肺IL-1βmRNA、IL-18 mRNA和TNF-αmRNA的表达分别与N组、NS组、A组比较差异有统计学意义(P<0.05),A组小鼠血清IL-18水平高于其他3组,分别与N组、NS组、J组比较差异有统计学意义(P<0.05)。结论激活α7nAChR可以直接抑制肺组织CD11b的释放,减少炎症因子的集聚;同时还可以直接抑制肺组织炎症因子IL-1βmRNA、IL-18m RNA和TNF-αmRNA的表达和IL-18的释放,从而抑制ARDS的炎症反应,减轻ARDS病理变化。Objective To investigate the effects ofα7 nicotinic acetylcholine receptor(α7nAChR)on CD11b,IL-1β,IL-18 and TNF-αin acute respiratory distress syndrome(ARDS)mice.Methods A total of 40 healthy and clean male Balb/C mice(6 weeks old)were randomly divided into normal group(N group),normal saline control group(NS group),ARDS group(A group),and ARDS mice treated with nicotinic acetylcholine receptor agonist after bilateral cervical vagotomy group(J group),with 10 mice in each group.The right lung structure of mice in each group was observed by hematoxylin-eosin(HE)staining,the lung tissue wet weight/body weight ratio(LWW/DW ratio)was detected,and the percentage of CD11b in the alveolar lavage fluid of mice was detected by flow cytometry.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)was used to detect the expression of IL-1βmRNA,IL-18 mRNA and TNF-αmRNA in left lung tissue.Serum IL-18 was determined by enzyme-linked immunosorbent assay(ELISA)and double antibody sandwich method.Results HE staining of the right lung of mice in group N and NS showed normal structure,while the lung interstitial of mice in group A showed a large number of inflammatory cells infiltrated,alveolar wall thickened,alveolar structure destroyed and alveolar cavity fused.The alveolar structure of mice in group J was intact,with a little damage and alveolar cavity.The percentage of CD11b in alveolar lavage fluid in group A was higher than that in the other three groups,and the difference was statistically significant compared with group N,NS and J,respectively(P<0.05).The expressions of IL-1βmRNA,IL-18 mRNA and TNF-αmRNA in the left lung of mice in group J were statistically significant compared with those in group N,NS and A(P<0.05),and the serum IL-18 level of mice in group A was higher than that in the other three groups,and the differences were statistically significant compared with groups N,NS and J,respectively(P<0.05).Conclusions Activation ofα7nAChR can directly inhibit the release of CD11b in lung tissue an

关 键 词：α7亚单位的N型乙酰胆碱受体 CD11B 白细胞介素-1Β 白细胞介素-18 肿瘤坏死因子-Α 

分 类 号：R563.9[医药卫生—呼吸系统]