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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 investigate the proinflammatory effect of interleukin (IL) -36α in autoimmune myocarditis (AMC) mice. Methods: Forty BALB / c mice were randomly divided into control group, experimental group (including AMC group, AMC + IL-36α group and AMC + IL-36Ra group). Experimental group was established experimental AMC animal model, The mice were injected intraperitoneally with IL-36α and IL-36Ra respectively for 7 days on the 15th day after modeling. The hearts of mice were examined by echocardiography on the 21st day. Serum inflammatory cytokines IL-23 and IL- 17 concentration; hematoxylin-eosin (HE) staining examination of myocardial pathology. Results: Compared with the control group, the mice in the experimental group showed varying degrees of cardiac insufficiency, serum IL-23 and IL-17 levels were significantly increased, inflammatory cell infiltration was found in the pathological sections of the myocardium, and AMC + IL-36α group Mice inflammatory factors increased, inflammatory cell infiltration increased and cardiac dysfunction was the most obvious, while the AMC + IL-36Ra group than the AMC group, the indicators were significantly inhibited, the differences between the groups were statistically significant ( P <0.05). Conclusion: IL-36α has a proinflammatory effect in myocardium of AMC mice. Suppression of IL-36α expression can reduce the progression of AMC.