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作 者:王子萌[1] 王维[1] 马毓蓉 范芳梅 金春芳 黄益飞[1] 项云[1] 刘佳丽[1] 何於娟[1]
机构地区:[1]重庆医科大学检验医学院临床检验诊断学教育部重点实验室,400016
出 处:《免疫学杂志》2017年第3期208-213,共6页Immunological Journal
基 金:国家自然科学基金(csfc81373151);重庆市教委科学技术研究项目(KJ130313)
摘 要:目的建立肺炎链球菌性急性中耳炎小鼠模型,研究白细胞介素17A(interleukin 17A,IL-17A)促进中耳上皮细胞凋亡以及凋亡促进中耳组织损伤的作用。方法鼓膜穿刺术建立C57BL/6小鼠和IL-17A缺陷鼠急性中耳炎模型。收集中耳灌洗液,ELISA检测灌洗液中炎症因子和损伤标志物的表达。中耳组织石蜡切片经TUNEL染色和HE染色,观察小鼠中耳上皮细胞的凋亡和中耳组织损伤程度。采用广谱的凋亡抑制剂Z-VAD-FNK抑制凋亡后,观察中耳组织损伤的变化。结果 IL-17A显著上调白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)和髓过氧化物酶(MPO)表达,加重了中耳炎症。IL-17A还促进了上皮细胞的凋亡和黏膜损伤。抑制凋亡后,显著降低了IL-17A介导的炎症反应,减轻了中耳组织损伤。结论 IL-17A可促进上皮细胞凋亡,加重中耳组织损伤。To study the role of IL-17 A in promoting epithelial apoptosis and tissue injury, we developed a mouse model of acute otitis media(AOM) by direct transtympanic inoculation with Streptococcus pneumoniae(S. pn).Middle ear lavage fluid(MELF) and middle ears(ME) tissues were collected from C57BL/6 mice and IL-17A^-/-mice at day 3 after S. pn inoculation. Then the expression levels of IL-6 and TNF-α were analyzed by ELISA method;myeloperoxidase(MPO) activity was measured by the MPO activity assay. The ME tissues were collected for HE and TUNEL staining. Data showed that IL-17 A induced epithelial apoptosis and tissue injury, as well as aggravated the ME inflammation by increasing the levels of IL-6, TNF-α and MPO. Reversely, the injection of caspase inhibitor Z-VAD-FMK significantly restrained the tissue injury of OM by decreasing the levels of IL-6, TNF-α and MPO.These data supports the conclusion that IL-17 A aggravates tissue injury of ME through promoting epithelial apoptosis.
分 类 号:R764.21[医药卫生—耳鼻咽喉科] R446[医药卫生—临床医学]
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