首页> 中文期刊> 《中国生化药物杂志 》 >脂肪细胞因子对大鼠肥胖哮喘模型免疫应激功能的影响

脂肪细胞因子对大鼠肥胖哮喘模型免疫应激功能的影响

             

摘要

目的 探讨脂肪细胞因子对肥胖哮喘模型大鼠的免疫应激功能的影响.方法 C57BL/6J小鼠40只,随机均分成对照组、单纯肥胖组、单纯哮喘组和肥胖哮喘组,对照组小鼠喂养普通饲料和PBS,单纯肥胖组小鼠喂养高脂饲料(75%普通饲料,10%蛋黄粉,10%猪油,5%白糖)和PBS;单纯哮喘组小鼠喂养普通饲料和OVA(PBS)致敏激发;肥胖哮喘组小鼠喂养高脂饲料和OVA(PBS)致敏激发.末次激发结束后使用酶联免疫吸附剂测定(enzyme-linked immunosorbent assay, ELISA法检测血浆和支气管肺泡灌洗液(BALF)中的瘦素(leptin)、脂联素(adiponectin)、抵抗素(resistin)、IL-4、IFN-γ、IL-17的蛋白含量.并使用Pearson相关性分析评价这些因子在血浆和BALF中的水平的相关性.结果 不同组小鼠血浆中的瘦素、脂联素、抵抗素的差异有统计学意义(P<0.05);不同组小鼠BALF中脂联素、抵抗素差异有统计学意义(P<0.05),瘦素差异没有统计学意义;肥胖小鼠血浆和BALF中瘦素含量均明显升高,且两者呈现正相关性(R2=0.8215,P<0.05),脂联素、抵抗素在血浆和BALF中的含量没有相关性(P>0.05);BALF中脂联素含量与IFN-γ水平也呈负相关(R2=0.9146,P<0.05),而瘦素、脂联素、抵抗素与IL-4、IL-17之间没有相关性.结论 脂肪细胞因子对肥胖哮喘模型大鼠的免疫应激功能具有调控作用,参与抗炎反应.%Objective To study the Inflammation and immune stress of obese asthmatic rats by adipocytokines.Methods Fourty C57BL/6 J mice were randomly divided into control group, obese group, asthma group and obese asthma group.Mice in the control group were fed normal diet and PBS, high-fat diet(75% normal diet, 10% egg yolk powder, lard 10%, 5% sugar)and PBS in obese group, normal diet and OVA(PBS)in asthma group and fat diet and OVA(PBS)in obese asthma group.Detect the leptin, adiponectin, resistin, IL-4, IFN-γ, IL-17 content with ELISA in serum and bronchoalveolar lavage fluid(BALF).Using Pearson correlation to analyze and evaluate these factors' correlation in plasma and BALF.Results The difference of leptin, adiponectin, resistin in plasma and BALF(excepted leptin)between four groups were statistically significant (P<0.05), the leptin levels between plasma and BALF has a positive correlation(R2=0.8215, P<0.05)in obese mice, there was no correlation between plasma and BALF for the adiponectin, resistin.The adiponectin content and IFN-γ levels were also negatively correlated(R2=0.9146, P<0.05)in BALF, while there was no correlation between IL-4,IL-17 and leptin, adiponectin, resistin.Conclusion Adipocytokines has a regulatory function of the immune response in obese asthmatic rats, and participate the inflammatory reaction.

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