Gillespie Kevin, Kodani Isamu, Dickinson Douglas P, Ogbureke Kalu U E, Camba Amy M, Wu Mengjie, Looney Stephen, Chu Tin-Chun, Qin Haiyan, Bisch Frederick, Sharawy Mohamed, Schuster George S, Hsu Stephen D
Department of Periodontology, US Army Fort Gordon, Fort Gordon, GA, USA.
Life Sci. 2008 Oct 24;83(17-18):581-8. doi: 10.1016/j.lfs.2008.08.011. Epub 2008 Sep 6.
Protection of glandular cells from autoimmune-induced damage would be of significant clinical benefit to Sjogren's syndrome (SS) patients. Epigallocatechin-3-gallate (EGCG) possesses anti-apoptotic, anti-inflammatory, and autoantigen-inhibitory properties.
To investigate if EGCG protects against certain autoimmune-induced pathological changes in the salivary glands of the non-obese diabetic (NOD) mouse model for SS.
Animals were provided with either water or water containing 0.2% EGCG. At the age of 8, 16 and 22 weeks, submandibular salivary gland tissue and serum samples were collected for pathological and serological analysis.
Significant lymphocyte infiltration was observed in the salivary glands of the water-fed group at the age of 16 weeks, while the EGCG group showed reduced lymphocyte infiltration. By 22 weeks of age, water-fed animals demonstrated elevated levels of apoptotic activity within the lymphocytic infiltrates, and high levels of serum total anti-nuclear antibody, compared to EGCG-fed animals. Remarkably, proliferating cell nuclear antigen (PCNA) and Ki-67 levels in the salivary glands of water-fed NOD mice were significantly elevated in comparison to BALB/c control mice; in contrast, PCNA and Ki-67 levels in EGCG-fed NOD animals were similar to BALB/c mice. These results indicate that EGCG protects the NOD mouse submandibular glands from autoimmune-induced inflammation, and reduces serum autoantibody levels. Abnormal proliferation, rather than apoptosis, appears to be a characteristic of the NOD mouse gland that is normalized by EGCG. The evidence suggests that EGCG could be useful in delaying or managing SS-like autoimmune disorders.
保护腺细胞免受自身免疫诱导的损伤对干燥综合征(SS)患者具有重大临床益处。表没食子儿茶素-3-没食子酸酯(EGCG)具有抗凋亡、抗炎和抑制自身抗原的特性。
研究EGCG是否能预防非肥胖糖尿病(NOD)小鼠干燥综合征模型唾液腺中某些自身免疫诱导的病理变化。
给动物提供水或含0.2%EGCG的水。在8、16和22周龄时,收集下颌下唾液腺组织和血清样本进行病理和血清学分析。
在16周龄时,饮水组小鼠的唾液腺中观察到明显的淋巴细胞浸润,而EGCG组的淋巴细胞浸润减少。到22周龄时,与饮用EGCG水的动物相比,饮水动物淋巴细胞浸润内的凋亡活性水平升高,血清总抗核抗体水平也较高。值得注意的是,与BALB/c对照小鼠相比,饮水的NOD小鼠唾液腺中的增殖细胞核抗原(PCNA)和Ki-67水平显著升高;相比之下,饮用EGCG水的NOD动物的PCNA和Ki-67水平与BALB/c小鼠相似。这些结果表明,EGCG可保护NOD小鼠下颌下腺免受自身免疫诱导的炎症,并降低血清自身抗体水平。异常增殖而非凋亡似乎是NOD小鼠腺体的一个特征,而EGCG可使其恢复正常。有证据表明,EGCG可能有助于延缓或控制类似SS的自身免疫性疾病。