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(-)-表没食子儿茶素-3-没食子酸酯通过抗炎、抗凋亡及抑制TRAIL信号通路对大鼠自身免疫性甲状腺炎的神经保护作用

Neuroprotective effect of (-)-epigallocatechin-3-gallate on autoimmune thyroiditis in a rat model by an anti-inflammation effect, anti-apoptosis and inhibition of TRAIL signaling pathway.

作者信息

Li Junfeng

机构信息

Department of Endocrinology and Metabolism, The First Center Hospital of Tianjin, Tianjin 300000, P.R. China.

出版信息

Exp Ther Med. 2018 Jan;15(1):1087-1092. doi: 10.3892/etm.2017.5511. Epub 2017 Nov 14.

Abstract

(-)-Epigallocatechin-3-gallate (EGCG) is a polyphenol monomer compound extracted and separated from green tea, and is a key catechin in green tea. Recent research has identified that EGCG is equipped with important biological activities, including antitumor, antioxidant, anti-inflammation, blood fat reduction and radiation protection abilities. In the current study, it was investigated whether EGCG exerts a neuroprotective effect on AIT and examined the possible underlying mechanism. The present study sought to establish an experimental autoimmune thyroiditis (AIT) rat model and to investigate the neuroprotective effect of EGCG in this model. EGCG was demonstrated to inhibit urinary iodine values and thyroid pathological features in AIT model rats. Treatment with EGCG significantly reduced interleukin-1β, interferon-γ (INF-γ) and tumor necrosis factor-α (TNF-α) levels in the AIT rats through suppression of nuclear factor-κB (NF-κB) pathway. In addition, pretreatment with EGCG significantly increased B-cell lymphoma-2 protein expression, and suppressed caspase-3 activity and TNF-α-related apoptosis-inducing ligand (TRAIL) protein expression levels in the AIT model rats. In conclusion, these results suggested that the neuroprotective effect of EGCG protects against AIT through its anti-inflammatory ability, anti-apoptosis and TRAIL signaling pathway in model rats, and it may be used as a therapeutic agent against AIT caused by inflammation.

摘要

(-)-表没食子儿茶素-3-没食子酸酯(EGCG)是从绿茶中提取分离得到的一种多酚单体化合物,是绿茶中的关键儿茶素。最近的研究发现,EGCG具有重要的生物活性,包括抗肿瘤、抗氧化、抗炎、降血脂和辐射防护能力。在本研究中,研究了EGCG是否对自身免疫性甲状腺炎(AIT)发挥神经保护作用,并探讨了可能的潜在机制。本研究旨在建立实验性自身免疫性甲状腺炎(AIT)大鼠模型,并研究EGCG在该模型中的神经保护作用。结果表明,EGCG可抑制AIT模型大鼠的尿碘值和甲状腺病理特征。EGCG治疗通过抑制核因子-κB(NF-κB)途径显著降低了AIT大鼠白细胞介素-1β、干扰素-γ(INF-γ)和肿瘤坏死因子-α(TNF-α)水平。此外,EGCG预处理显著增加了AIT模型大鼠B细胞淋巴瘤-2蛋白表达,抑制了半胱天冬酶-3活性和TNF-α相关凋亡诱导配体(TRAIL)蛋白表达水平。总之,这些结果表明,EGCG的神经保护作用通过其抗炎能力、抗凋亡作用以及在模型大鼠中的TRAIL信号通路来预防AIT,它可能用作治疗炎症引起的AIT的药物。

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