| 吴可人.大黄素对实验性自身免疫性甲状腺炎小鼠T细胞亚群和IFN-γ、IL-4分泌能力的影响[J].浙江中西医结合杂志,2017,27(11): |
| 大黄素对实验性自身免疫性甲状腺炎小鼠T细胞亚群和IFN-γ、IL-4分泌能力的影响 |
| Effects of emodin on T cell subsets and the IFN-γ, IL-4 secretion ability in experimental autoimmune thyroiditis mice |
| 投稿时间：2017-04-24 修订日期：2017-05-24 |
| DOI： |
| 中文关键词: 实验性自身免疫性甲状腺炎 大黄素 T细胞亚群 NOD小鼠 |
| 英文关键词:experimental autoimmune thyroiditis Emodin T cell subsets NOD mice |
| 基金项目:浙江省中医药科技计划资助（2014ZA037） |
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| 中文摘要: |
| 目的：大黄素对实验性自身免疫性甲状腺炎小鼠的保护和机制研究。方法：通过过量碘剂诱导 NOD 小鼠建立EAT动物模型，造模4周后各实验组摄入不同剂量的大黄素。造模8 周后检测小鼠血浆TgAb 水平及甲状腺炎症程度以观察大黄素的保护作用。流式细胞术检测小鼠外周血、脾脏 T 细胞亚群，分析大黄素对EAT小鼠外周血、脾脏淋巴细胞IFN-γ和IL-4分泌能力的影响。结果:（1）甲状腺病理学观察，大黄素实验组较模型组甲状腺淋巴细胞浸润程度减轻；分级比较有显著性差异（P<0.01）；（2）造模后各组小鼠血浆TgAb水平明显升高（44.16±3.59 vs 11.24±1.52），大黄素实验组升高幅度低于模型组（26.58±5.24，19.18±5.73，23.24±5.47 vs 44.16±3.59），各组间有统计学差异(P<0.01)；（3）大黄素实验组外周血单核细胞、脾脏淋巴细胞中 CD3+CD4+、CD3+CD8+T淋巴细胞的频率较对照组明显升高（外周血单核细胞7.72±2.92 vs 4.13±1.45，4.23±1.58 vs 2.76±1.69；脾脏淋巴细胞7.51±1.31 vs 1.82±1.35，5.59±1.98 vs 0.033±0.034），但低于模型组（外周血单核细胞7.72±2.92 vs 17.46±3.71，4.23±1.58 vs 8.92±2.62；脾脏淋巴细胞7.51±1.31 vs 16.74±4.79，5.59±1.98 vs 11.97±2.21）（P<0.01）；而CD3+CD4+FIN-γ+、CD3+CD4+IL-4+T细胞频率高于对照组但明显低于模型组（P<0.01）。结论：过量碘剂诱导NOD小鼠自身免疫性甲状腺炎造模是可行的；大黄素对造模小鼠甲状腺炎有一定保护作用。大黄素通过抑制CD4+、CD8+T淋巴细胞分化并且抑制IFN-γ和IL-4的分泌，从而抑制造模小鼠的自身免疫反应。 |
| 英文摘要: |
| Objective: To investigate the protective effect of emodin on thyroid in experimental autoimmune thyroiditis (EAT) mice and its mechanism.
Methods: Four weeks after modeling, experimental groups were treated with emodin with different doses. The TgAb level in plasma and thyroid inflammation were detected eight weeks after modeling to evaluate the protective effect of emodin on EAT mice. T cell subset in peripheral blood and spleen were detected by flow cytometry.Results: （1）The histopathological study revealed that inflammatory infiltration in thyroid was significant reduced compared with control group (P<0.01).（2）Levels of plasma TgAb were significant increased in each group after modeling(44.16±3.59 vs 11.24±1.52), and the increasing amplitudes in emodin treated groups were significantly less than that in model group（26.58±5.24，19.18±5.73，23.24±5.47 vs 44.16±3.59） (P<0.01). （3）After modeling, the cell frequencies of CD3+CD4+, CD3+CD8+T cells, CD3+CD4+IL-4+ and CD3+CD4+IFN-γ+ T cells, in peripheral blood monocyte and splenic lymphocyte were significant increased in each group compared with the control group （peripheral blood monocyte:7.72±2.92 vs 4.13±1.45，4.23±1.58 vs 2.76±1.69;splenic lymphocyte:7.51±1.31 vs 1.82±1.35，5.59±1.98 vs 0.033±0.034）(P<0.01).While the increasing amplitudes in emodin treated groups were less than that in model group（peripheral blood monocyte:7.72±2.92 vs 17.46±3.71，4.23±1.58 vs 8.92±2.62;splenic lymphocyte :7.51±1.31 vs 16.74±4.79，5.59±1.98 vs 11.97±2.21）. The cell frequencies of CD3+CD4+FIN-γ+ and CD3+CD4+IL-4+T cells in emodin treated groups were significant higher than control group and lower than model groups. （P<0.01）
Conclusion: The EAT model is visible which though an excessive iodine-induced method in NOD mice, and emodin shows a certain inhibitory effect on autoimmune response in EAT mice. This effect could be performed by inhibiting the differentiation of lymphocyte into CD3+CD4+, CD3+CD8+T cells and by inhibiting the secretion of IFN-γ and IL-4 in CD3+CD4+ T cells, thereby inhibite the autoimmune response in EAT mice. |
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