EMAP-Ⅱ及TNF-α炎症通路在无菌性脑炎致病机制中的作用

Role of EMAP- Ⅱ and TNF-α inflammatory pathways in aseptic encephalitis pathogenesis

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.