摘要
目的探讨白细胞介素-11(interleukin-11,IL-11)在小鼠脑缺血再灌注损伤中的保护作用及机制研究。方法选择SPF级C57BL/6雄性小鼠60只,随机分成为对照组、模型组和IL-11组,每组各20只,通过线栓法构建脑缺血再灌注损伤。应用TTC染色检测脑组织梗死面积,采用Longa评分法评估各组小鼠的神经功能,检测并计算各组小鼠的脑组织含水量。应用Western blot法检测脑组织诱导型一氧化氮合酶(iNOS)、IL-1β、CD206和精氨酸酶(Arginase)-1蛋白表达水平。应用酶联免疫吸附(ELISA)法检测IL-1、IL-6、IL-10和肿瘤坏死因子(TNF)-α水平。免疫荧光双染检测IL-11对小胶质细胞分化的影响。结果与对照组比较,模型组小鼠脑组织梗死面积、含水量和Longa评分均显著升高(均P<0.05);与模型组比较,IL-11组小鼠脑组织梗死面积、含水量和Longa评分均显著减低(均P<0.05);与对照组比较,模型组小鼠M1型小胶质细胞数量明显升高(均P<0.05);与模型组比较,IL-11组小鼠M1型小胶质细胞数量降低,M2型小胶质细胞数量升高(均P<0.05);与对照组比较,模型组小鼠M1型小胶质细胞标记物iNOS和IL-1β表达升高(均P<0.05);与模型组比较,IL-11组小鼠M1型小胶质细胞标记物iNOS和IL-1β表达降低,M2型小胶质细胞标记物CD206和Arginase-1表达升高(均P<0.05);与对照组比较,模型组小鼠脑组织IL1、IL-6、TNF-α水平明显升高,IL-10水平明显降低(均P<0.05);与模型组比较,IL-11组小鼠脑组织IL-1、IL-6和TNF-α水平明显降低,IL-10水平明显升高(P<0.05)。结论IL-11促进小胶质细胞由促炎表型M1型向抗炎表型M2型转化,降低脑组织炎症,发挥脑缺血保护作用。
To investigate the protective effects of interleukin-11(IL-11)against cerebral ischemia reperfusion injury and the mechanism in mice,total of 60 male C57BL/6J mice were recruited and randomly divided into control group,model group and IL-11 group,with 20 mice in each group.The middle cerebral artery occlusion models were established.TTC staining was used to observe the area of cerebral infarction;Longa grade method was used to evaluate the neurobehavioral characteristics of mice,and the water content of brain tissue was measured.The expression levels of iNOS,IL-1β,CD206 and Aginase-1 in brain tissue were detected by Western blotting and the expression levels of IL-1,IL-6,IL-17 and TNF-αwere detected by ELISA.Immunofluorescence double staining was used to detect the effect of IL-11 on the differentiation of microglia.Compared with the control group,the area of cerebral infarction,Longa grade and the water content of brain tissue were significantly increased in model group.Meanwhile,those parameters were significantly decreased in IL-11 group.Compared with the control group,the number of M1 microglia in the model group was significantly increased;compared with the model group,the number of M1 microglia in the IL-11 group was decreased,and the number of M2 microglia was increased.Compared with the control group,the expression of type M1 microglia markers iNOS and IL-1βwere increased in the model group;compared with the model group,the expression of type M1 microglia markers iNOS and IL-1βwere decreased,while the expression of type M2 microglia markers CD206 and Aginase-1 were increased in the IL-11 group.Compared with the sham group,the levels of IL-1,IL-6,and TNF-αwere significantly increased,but IL-10 was significantly decreased in model group.Compared with the model group,the levels of IL-1,IL-6,and TNF-αwere significantly decreased,but IL-10 was significantly increased in IL-11 group.In conclusion,IL-11 promotes the transformation of microglia from pro-inflammatory phenotype M1 to anti-inflammatory phenoty
作者
张玉敏
韩素桂
刘启为
周琪
卢军利
ZHANG Yumin;HAN Sugui;LIU Qiwei;ZHOU Qi;LU Junli(Department of Clinical Laboratory,Tangshan People’s Hospital,Tangshan 063000,China;Department of Nuclear Medicine,Tangshan People’s Hospital,Tangshan 063000,China;Department of Neurology,Tangshan People’s Hospital,Tangshan 063000,China;Department of Emergency,Tangshan People’s Hospital,Tangshan 063000,China)
出处
《免疫学杂志》
CAS
CSCD
北大核心
2021年第2期134-139,共6页
Immunological Journal
基金
2017年度河北省医学科学研究重点课题(20171295)。
