首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >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
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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

机译:(-)-epigallocatechin-3-gallate对大鼠模型自身免疫性甲状腺炎的抗炎作用抗凋亡和TRAIL信号通路抑制作用的神经保护作用

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摘要

(−)-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.
机译:(-)-Epigallocatechin-3-gallate(EGCG)是从绿茶中提取并分离出的多酚单体化合物,是绿茶中的关键儿茶素。最近的研究发现,EGCG具有重要的生物学活性,包括抗肿瘤,抗氧化剂,抗炎,降低血脂和辐射防护能力。在当前的研究中,研究了EGCG是否对AIT发挥了神经保护作用,并研究了可能的潜在机制。本研究试图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。事实证明,EGCG可抑制AIT模型大鼠的尿碘值和甲状腺病理特征。 EGCG处理可通过抑制核因子-κB(NF-κB)通路显着降低AIT大鼠的白介素-1β,干扰素-γ(INF-γ)和肿瘤坏死因子-α(TNF-α)水平。此外,在AIT模型大鼠中,EGCG预处理可显着增加B细胞淋巴瘤2蛋白表达,并抑制caspase-3活性和TNF-α相关的凋亡诱导配体(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在模型大鼠中的抗炎能力,抗凋亡和TRAIL信号传导途径来预防AIT,并且可以用作针对由炎症引起的AIT的治疗剂。

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