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机构地区:[1]广州医科大学附属脑科医院神经内科,广东省510370
出 处:《中华临床医师杂志(电子版)》2015年第7期16-18,共3页Chinese Journal of Clinicians(Electronic Edition)
摘 要:目的探讨内皮-单核细胞激活多肽酶Ⅱ(EMAP-Ⅱ)及TNF-α炎症通路在无菌性脑炎致病机制中的作用。方法收集2013~2014年我院确诊为无菌性脑炎的43例患者血清标本,用ELISA的方法半定量检测EMAP-Ⅱ、TNF-α的表达,用比色法测定超氧化物歧化酶(SOD)水平。比较无菌性脑炎患者治疗前后外周血中EMAP-Ⅱ的表达变化及与TNF-α、SOD水平的相关性。结果(1)无菌性脑炎患者外周血中EMAP-Ⅱ水平较正常人明显升高,并于治疗后明显下降,但仍高于正常水平;(2)无菌性脑炎患者外周血中EMAP-Ⅱ水平与TNF-α水平呈明显正相关,与SOD水平呈明显负相关。结论 EMAP-II及TNF-α炎症通路可能参与了无菌性脑炎的致病。Objective To explore the role of EMAP- Ⅱ(endothelial-monocyte activating polypeptide- Ⅱ) and TNF-α inflammatory pathways in pathogenesis of aseptic meningitis. Methods 43 cases of aseptic meningitis were collected to take serum samples in our hospital during 2013-2014, ELISA method was used for semi-quantitative detection of the expression of EMAP- Ⅱ and TNF-α, and chromatometry method was used for determination of SOD(super oxide colorimetric) levels. Expression level of EMAP-Ⅱ in peripheral blood of aseptic meningitis patients before and after the treatment and the correlation of EMAP-Ⅱ with TNF-α, SOD levels were compared. Results(1) EMAP-Ⅱ levels of blood in patients with aseptic meningitis were significantly higher than normal, and were significantly decreased after treatment, but still higher than the normal level;(2) EMAP-Ⅱ levels of blood in patients with aseptic meningitis were significantly positively correlated with the level of TNF-α and negatively correlated with the level of SOD. Conclusion EMAP- Ⅱ and TNF-α inflammatory pathways may be involved in the pathogenesis of aseptic meningitis.
关 键 词:肿瘤坏死因子α 脑膜炎 无菌性 EMAP-Ⅱ 致病机制
分 类 号:R742.9[医药卫生—神经病学与精神病学]
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