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作 者:张杰波 刘映峰[1] 林湧滦 游伟[1] 缪绯[1] 刘芃[1]
机构地区:[1]南方医科大学珠江医院心血管内科,广州510282
出 处:《临床心血管病杂志》2015年第6期659-663,共5页Journal of Clinical Cardiology
基 金:广东省自然科学基金(No:10151051501000038);广东省科技计划项目(No:20130319c)
摘 要:目的:探讨白细胞介素(IL)-36α在自身免疫性心肌炎(AMC)小鼠中的促炎作用。方法:将40只BALB/c小鼠随机分为对照组、实验组(包括AMC组、AMC+IL-36α组和AMC+IL-36Ra组),实验组构建实验性AMC动物模型,后两组小鼠在造模第15天,分别予IL-36α和IL-36Ra连续腹腔注射7d,于第21天行小鼠心脏超声检查,酶联免疫吸附法测定血清炎性因子IL-23、IL-17浓度;苏木精-伊红(HE)染色检查心肌病理改变。结果:与对照组相比,实验组小鼠出现不同程度的心功能不全,血清IL-23、IL-17水平明显增高,心肌病理切片可见炎性细胞浸润,其中又以AMC+IL-36α组小鼠炎性因子上升、炎性细胞浸润增加及心功能不全最明显,而较AMC组,AMC+IL-36Ra组小鼠的各项指标被显著抑制,各组间差异均有统计学意义(P<0.05)。结论:IL-36α在小鼠AMC心肌组织中具有促炎作用,抑制IL-36α的表达可减轻AMC的进展。Objective:To discuss the proinflammatory role of IL-36αin autoimmune myocarditis(AMC)in mice.Method:The 40BALB/c mice were randomly divided into control(Ctrl)group,the experimental group(including AMC,AMC+IL-36αGroup and AMC+IL-36 Ra group).The experimental autoimmune myocarditis model were constructed in the experimental group(EAM).After the first 15 days of modeling,the later two groups of the experimental group were given IL-36αand IL-36 Ra by intraperitoneal injection from 16d-21 d.In the 21 d,echocardiography was used to exam the cardiac function of mice,and Enzyme-linked immunosorbent assay was used to measure the concentration of serum inflammatory cytokines IL-23,IL 17.The cardiac pathology was checked by the HE staining.Result:Compared with the Ctrl group,the experimental group of mice have showed varying degrees of heart failure,and the level of IL-23,IL-17 in serum were significantly higher.Also the myocardial biopsy showed infiltration of inflammatory cells.Among them,the AMC + IL-36αgroup was the most obvious increase.However,The indicators of AMC+IL-36 Ra group was significantly inhibited.Differences between the groups were significant statistically(P〈0.05).Conclusion:IL-36αhas a proinflammatory role in myocardial tissue of AMV mice,which can reduce the advances of AMC.
关 键 词:白介素-36α 白介素-36Ra 自身免疫性心肌炎 小鼠
分 类 号:R542.2[医药卫生—心血管疾病]
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