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作 者:张红叶[1] 宋佳贤[1] 杨莉亚[1] 杨八双 黄旭[1] 董榕[2]
机构地区:[1]东南大学医学院 [2]东南大学生理教研室,江苏南京210009
出 处:《基础医学与临床》2011年第10期1099-1103,共5页Basic and Clinical Medicine
基 金:国家大学生创新性实验计划项目(G2007061)
摘 要:目的探讨中枢组胺在心理应激致大鼠哮喘发病中的中枢免疫调节作用及其机制。方法 SD大鼠随机分为5组(每组n=10):对照组、哮喘组、应激组、应激哮喘组及侧脑室注射扑尔敏组,测定肺通气功能,放免法测定血清皮质酮(CORT)含量,ELISA测定IL-4及IFN-γ水平,并计算Th1/Th2比值;HE染色观察肺组织形态;高效液相法测定下丘脑内组胺含量;侧脑室注射H1受体拮抗剂扑尔敏观察应激哮喘组肺通气功能、Th1/Th2比值的变化。结果与哮喘组相比:应激哮喘组肺通气功能下降(P<0.05);血清Th1/Th2比值下降(P<0.05),肺组织炎性浸润加重;下丘脑内组胺从231±32 nmol/g升高至287±44 nmol/g(P<0.05)。侧脑室注射H1受体拮抗剂扑尔敏后可减轻上述变化。结论心理应激可致哮喘大鼠中枢组胺含量升高,后者作用于H1受体,加重哮喘气道高反应性及气道炎性反应。Objective This study aims to investigate the mechanism of central histamine on psychological stress rats with asthma.Methods Healthy SD rats were randomly assigned as 4 test groups and me control group.Asthma and psychological stress rat models were established.Pulmonary function was tested by Powlab biological signal processing system.Serum corticosterone(CORT) was tested by radioimmunoassay.Serum IL-4,IFN-γ were tested by enzyme-linked immunosorbent assay,which were used to calculate the ratio of Th1/Th2.Lung tissues were stained with HE.Histamine content in the hypothalamus was determined by HPLC.And through intracerebroventricular injection of histamine H1 receptor antagonist,chlorpheniramine,to observe pulmonary function and Th1/Th2 ratio in rats with asthma.Results After the psychological stress,compared with the asthma model group,pulmonary function of stress asthmatic rats decreased(P0.05).Serum Th1/Th2 ratio were decreased(P0.05).Besides,peripheral inflammation of lung tissue were worse.Histamine in the hypothalamus was increased from 231±32 nmol/g to 287±44 nmol/g(P0.05).However,after intracerebroventricular injection of histamine H1 receptor antagonist,chlorpheniramine,pulmonary dysfunction of the stressed asthmatic rats and inflammation of lung tissue were improved.Conclusions Psychological stress can increase central histamine levels in rats with asthma,and elevated histamine acts on H1 receptors,that plays a important role in the pathogenesis of airway hyperresponsiveness and peripheral inflammation.
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