Literature DB >> 18809413

Effects of oral consumption of the green tea polyphenol EGCG in a murine model for human Sjogren's syndrome, an autoimmune disease.

Kevin Gillespie1, Isamu Kodani, Douglas P Dickinson, Kalu U E Ogbureke, Amy M Camba, Mengjie Wu, Stephen Looney, Tin-Chun Chu, Haiyan Qin, Frederick Bisch, Mohamed Sharawy, George S Schuster, Stephen D Hsu.   

Abstract

SIGNIFICANCE: 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. AIMS: 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. MAIN
METHODS: 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. KEY
FINDINGS: 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.

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Year:  2008        PMID: 18809413      PMCID: PMC2701648          DOI: 10.1016/j.lfs.2008.08.011

Source DB:  PubMed          Journal:  Life Sci        ISSN: 0024-3205            Impact factor:   5.037


  28 in total

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Authors:  Malin V Jonsson; Nicolas Delaleu; Karl A Brokstad; Ellen Berggreen; Kathrine Skarstein
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Authors:  L J Zhao; Z J Li; Y Y Huang; Z K Ti; Y Chen
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5.  Inhibition of autoantigen expression by (-)-epigallocatechin-3-gallate (the major constituent of green tea) in normal human cells.

Authors:  Stephen Hsu; Douglas P Dickinson; Haiyan Qin; Carol Lapp; David Lapp; James Borke; Douglas S Walsh; Wendy B Bollag; Hubert Stöppler; Tetsuya Yamamoto; Tokio Osaki; George Schuster
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7.  Salivary gland changes in the NOD mouse model for Sjögren's syndrome: is there a non-immune genetic trigger?

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8.  Green tea polyphenols reduce autoimmune symptoms in a murine model for human Sjogren's syndrome and protect human salivary acinar cells from TNF-alpha-induced cytotoxicity.

Authors:  Stephen D Hsu; Douglas P Dickinson; Haiyan Qin; James Borke; Kalu U E Ogbureke; Julia N Winger; Amy M Camba; Wendy B Bollag; Hubert J Stöppler; Mohamed M Sharawy; George S Schuster
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9.  [The effect of bakumondo-to on salivary secretion in Sjögren syndrome].

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2.  Epigallocatechin-3-gallate modulates anti-oxidant defense enzyme expression in murine submandibular and pancreatic exocrine gland cells and human HSG cells.

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6.  Epigallocatechin-3-gallate prevents autoimmune-associated down- regulation of p21 in salivary gland cells through a p53-independent pathway.

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9.  Green Tea Epigallocatechin-3-Gallate Suppresses Autoimmune Arthritis Through Indoleamine-2,3-Dioxygenase Expressing Dendritic Cells and the Nuclear Factor, Erythroid 2-Like 2 Antioxidant Pathway.

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Review 10.  Non-Nutrient, Naturally Occurring Phenolic Compounds with Antioxidant Activity for the Prevention and Treatment of Periodontal Diseases.

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