中文摘要：

目的探讨过氧化物酶体增殖物激活受体（PPAR）-γ对干燥综合征（ss）动物模型非肥胖型糖尿病（NOD）小鼠的抗炎作用。方法8周龄NOD小鼠20只，随机分为2组，每组10只。实验组自9周龄给予罗格列酮按40mg／kg剂量隔天灌胃。分别在12周龄和15周龄时随机处死罗格列酮组和对照组各1只小鼠，17周龄时处死全部小鼠，留取外周血和唇腺组织。用苏木素-伊红（HE）染色评价唇腺的病理学改变。酶联免疫吸附试验（ELISA）法测定外周血中自细胞介素（IL）-1β、IL-4、IL-6和肿瘤坏死因子（TNF）-α的含量。实时荧光定量反转录一聚合酶链反应（real—time PCR）检测唇腺组织中IL-1β、IL-4、IL-6和TNF-α mRNA的表达量。计量资料两样本间比较采用t检验。结果罗格列酮组小鼠唇腺组织中单核细胞浸润较对照组均减轻，腺体破坏少。17周龄时罗格列酮组与对照组比较，外周血IL-6[（26±7）与（37±11），t=-2．298]和TNF—α[（57±22）与（79±21），t=-2．188]的含量明显减少（P〈0．05）；IL-4[（26±13）与（12±4），t=2．438]的含量明显增加（P〈O．05）；唇腺组织中TNF-α mRNA的表达水平明显降低；而IL-4 mRNA的表达水平明显升高（P〈0.05）。结论PPAR-γ对NOD小鼠干燥综合征有疗效，其作用机制可能与其下调ss体内Thl细胞因子、使Th1/Th2平衡向Th2方向转化相关。

英文摘要：

Objective To investigate the anti-inflammatory effect of peroxisome proliferator-activated receptor-γ, （PPAR-γ） in non-obese diabetic mice （NOD mice） with SjGgren＇s syndrome （SS）. Methods Twenty 8-weeks-old female NOD mice were randomly divided into 2 groups. Rosiglitazone and normal saline were administered for the rosiglitazone group and control group respectively. At age of 12 weeks and 15 weeks, one mouse in the rosiglitazone group and the control group were killed respectively, and the others were sacrificed at the age of 17 weeks. Blood were obtained by cardiac puncture, and minor salivary glands （MSG） were resected. The histopathological changes waere examined by H＆E staining. The level of IL-1β, IL-4, IL-6 and TNF-α in sermn were measured by ELISA. Real-time PCR was used to evaluate the mRNA expression level of IL-1β, IL-4, IL-6 and TNF-α in MSG. Student＇s t-test was used to assess the differe- nces. Results Compared with the control group, the mice in the rosiglitazone group showed that： ①histo- patho-logical change was significantly ameliorated. ②At the age of 17 weeks, IL-6 [ （26±7） vs （37±11 ）, t=-2.298 ] and TNF-a [ （57±22） vs （79±21）, t=-2.188 ] were expressed significantly lower and IL-4 [ （26±13 ） vs （12±4）, t=2.438 ] was expressed significantly higher in serum （P〈0.05）. ③The expression of TNF-α was significantly decreased and the expression of IL-4 was significantly increased in MSG （P〈0.05）. Conclusion PPAR-γ can ameliorate SS on NOD mice effectively. The mechanism may be related toreduction of Thl cytokines, and the Thl/Th2 balance is changed into Th2 predominant.