多系统萎缩患者血清YKL-40和CD40水平变化及相关性因素研究Research on serum YKL-40,CD40 and relative factors in patients with multiple system atrophy
陈建文;周靖媛;张凯华;高松;赵莉;董春波;
摘要(Abstract):
目的探讨多系统萎缩(MSA)患者血清几丁质酶3样蛋白1(YKL-40)、CD40水平的变化,以及其与发病年龄、病程、疾病严重程度的相关性。方法病例组为2013-03-01—2014-11-30期间大连医科大学附属第一医院神经内科的住院MSA患者30例,其中很可能MSA24例,可能MSA6例,均符合2008年修订Gilman诊断标准;对照组为同期年龄和性别相匹配的30例健康体检者。利用酶联免疫吸附试验(ELISA)检测血清YKL-40与CD40水平,并分析两者与MSA患者性别、年龄、发病年龄、病程和疾病严重程度〔以统一多系统萎缩评估量表(UMSARS)Ⅱ评分进行评估〕的相关性。结果 MSA患者血清YKL-40水平〔38.32(11.74)ng/mL〕较对照组〔47.2(13.88ng/mL〕降低(t=238.00,P=0.002);对照组不同性别间〔男(36.23±9.74)ng/mL,女(36.50±10.86)ng/mL,t=0.519,P=0.477)〕及病例组不同分型间〔MSA-C型:40.67(13.09)ng/mL,MSA-P型:38.24(9.90)ng/mL,U=104.00,P=0.739〕比较血清YKL-40水平差异均无统计学意义。MSA患者血清中CD40水平〔120.39(39.47)pg/mL〕较对照组〔116.12(35.85)pg/mL〕差异无统计学意义(t=439.00,P=0.871)。对照组血清YKL-40水平与年龄无明显相关性(P>0.05),病例组血清YKL-40水平与患者发病年龄、病程和UMSARSⅡ评分均无相关性(均P>0.05);ROC曲线分析显示血清YKL-40水平对MSA无明确诊断价值(AUC=0.264,P=0.002)。结论 MSA患者血清YKL-40水平较健康人显著降低。MSA患者YKL-40水平与发病年龄、病程和UMSARSⅡ评分无相关性。
关键词(KeyWords): 多系统萎缩;血清YKL-40;血清CD40;生物标记物
基金项目(Foundation):
作者(Author): 陈建文;周靖媛;张凯华;高松;赵莉;董春波;
Email:
DOI:
参考文献(References):
- [1]Kragh CL,Gysbers AM,Rockenstein E,et al.Prodegenerative IkappaBalpha expression in oligodendroglial alpha-synuclein models of multiple system atrophy[J].Neurobiol Dis,2014,63:171-183.
- [2]Gilman S,Wenning G K,Low P A,et al.Second consensus statement on the diagnosis of multiple system atrophy[J].Neurology,2008,71(9):670-676.
- [3]Krismer F,Seppi K,Tison F,et al.The Unified Multiple System Atrophy Rating Scale:intrarater reliability[J].Mov Disord,2012,27(13):1683-1685.
- [4]Lindersson E,Lundvig D,Petersen C,et al.p25alpha Stimulates alpha-synuclein aggregation and is co-localized with aggregated alpha-synuclein in alpha-synucleinopathies[J].J Biol Chem,2005,280(7):5703-5715.
- [5]Papa S,Zazzeroni F,Pham CG,et al.Linking JNK signaling to NF-kappaB:a key to survival[J].J Cell Sci,2004,117(Pt22):5197-5208.
- [6]Shao R,Francescone R,Ngernyuang N,et al.Anti-YKL-40antibody and ionizing irradiation synergistically inhibit tumor vascularization and malignancy in glioblastoma[J].Carcinogenesis,2014,35(2):373-382.
- [7]Vinther-Jensen T,Budtz-Jorgensen E,Simonsen A H,et al.YKL-40in cerebrospinal fluid in Huntington's disease-A role in pathology or a nonspecific response to inflammation?[J].Parkinsonism Relat Disord,2014,20(11):1301-1303.
- [8]Bhat KP,Pelloski CE,Zhang Y,et al.Selective repression of YKL-40by NF-kappaB in glioma cell lines involves recruitment of histone deacetylase-1and-2[J].FEBS Lett,2008,582(21-22):3193-3200.
- [9]Recklies AD,Ling H,White C,et al.Inflammatory cytokines induce production of CHI3L1by articular chondrocytes[J].J Biol Chem,2005,280(50):41213-41221.
- [10]Francescone RA,Scully S,Faibish M,et al.Role of YKL-40in the angiogenesis,radioresistance,and progression of glioblastoma[J].J Biol Chem,2011,286(17):15332-15343.
- [11]Gorgens SW,Eckardt K,Elsen M,et al.Chitinase-3-like protein 1protects skeletal muscle from TNFalpha-induced inflammation and insulin resistance[J].Biochem J,2014,459(3):479-488.
- [12]Olsson B,Constantinescu R,Holmberg B,et al.The glial marker YKL-40is decreased in synucleinopathies[J].Mov Disord,2013,28(13):1882-1885.
- [13]Benveniste EN,Nguyen VT,Wesemann DR.Molecular regulation of CD40gene expression in macrophages and microglia[J].Brain Behav Immun,2004,18(1):7-12.
- [14]Goel C,Kalra N,Dwarakanath B S,et al.Per a 10protease activity modulates CD40expression on dendritic cell surface by NF-kappaB pathway[J].Clin Exp Immunol,2015,180(2):341-351.