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作 者:热孜万古丽·吾买尔[1] 斯拉甫·艾白[1] 艾克拜尔·安扎尔[1] 阿依努尔·艾买提[1]
机构地区:[1]新疆维吾尔自治区维吾尔医医院,国家中医药管理局维吾尔医皮肤病学重点学科,乌鲁木齐830049
出 处:《国际中医中药杂志》2012年第4期303-305,共3页International Journal of Traditional Chinese Medicine
基 金:国家自然科学基金项目(项目编号:81060314)
摘 要:目的探讨维吾尔医(简称“维医”)综合疗法对细胞因子免疫调节机制的影响。方法采用酶联免疫吸附试验(ELISA)测定80例寻常型银屑病患者维医综合治疗前后血清中干扰素(IFN-γ)、白细胞介素2(IL.2)、肿瘤坏死因子(TNF-α)及白细胞介素10(IL-10)、白细胞介素4(IL-4),并与60例健康成人进行对照。结果①患者组治疗前血清IFN_Y、IL.2、TNF-α水平高于对照组,其中IFN-y、IL-2与对照组比较,差异有统计学意义(纬烈。=0.043,PIL-2=0。008)IIL-10、IL-4水平低于对照组(地10=0.041,PⅡ4=0.049)。②治疗后,患者组IFN-γ、TNF-α、IL-10、IL-4与对照组比较,差异无统计学意义(PWN-γ=0.803,PTNF-γ=0.190,PIL-10=0.146,PIL-4=0.920),但IL-2高于对照组。结论维医综合治疗可改善Th1及Th2细胞分泌的细胞因子失衡。Objective To observe the changes of representative cytokine of Thl and Th2 cells in ordinary psoriasis patient's serum before and after the treatment of uygur medicine and to xplore its possible mechanism in the occurance of psoriasis. Methods Five cytokine including IFN-γ IL-2. TNF-α, IL-10, IL-4 in peripheral blood seruna of 80 ordinary psoriasis patient were assayed by enzyme linked immunosorbent assay (ELISA) before and after combined modality therapy of Uygur-medicine. 60 healthy volunteers were recurited for making a contrast. Results (1) before treatment, contrast to the healthy volunteer's, the IFN-γ, IL-2 and TNF-α levels of ordinary psoriasis patients were higher, in which, IFN-y and IL-2 had statistical significance(P〈0.001 ). While IL-10 and IL-4 were significantly lower than the healthy contrasts(Pmq0=0.041, Pm.4=0.049) ; (2) after the therapy, IFN-γ, IL-2, TNF-αIL-10 and IL-4 levels of ordinary psoriasis patients had no significant difference comparing to the healthy volunteer's (Pws.v=0.803, Pa-NF.a=0.190, PIL-100.146, PIL-4=0.920), but IL-2 level was significantly higher. Conclusion Unbalance of peripheral blood CD4+T cell subgroup (Th1/Th2) differentiation and their secretion cytokines are correlated to the initiation and development of ordinary psoriasis. Uygur-medicine combined modality therapy can significantly improve the unbalance status of cytokines secreted by Thl and Th2 cells.
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