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没食子儿茶素-3-没食子酸酯通过抑制 NLRP3 炎性小体激活预防炎症和糖尿病引起的葡萄糖耐量受损。

Epigallocatechin-3-gallate prevents inflammation and diabetes -Induced glucose tolerance through inhibition of NLRP3 inflammasome activation.

机构信息

Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.

Shandong Provincial Key Laboratory of Immunohematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.

出版信息

Int Immunopharmacol. 2021 Apr;93:107412. doi: 10.1016/j.intimp.2021.107412. Epub 2021 Jan 30.

DOI:10.1016/j.intimp.2021.107412
PMID:33524801
Abstract

Epigallocatechin-3-gallate (EGCG), the primary polyphenol component of green tea, has been shown to inhibit both oxidation and inflammation. However, the exact mechanism through which EGCG exhibits anti-inflammatory effects remains unclear. In this study, we assessed the potential pathways by which EGCG regulates NLRP3 inflammasome activity in vitro. We found that EGCG inhibits caspase-1 activation and IL-1β secretion by suppressing NLRP3 inflammasome activation in mouse bone marrow-derived macrophages (BMDMs). EGCG was also observed to block NLRP3-mediated ASC speckle formation and to alleviate pyroptosis in BMDMs. In addition, EGCG treatment could improve high-fat diet (HFD)-induced glucose tolerance and prevent NLRP3 inflammasome-dependent inflammation in a mouse model of HFD-induced type 2 diabetes (T2D). Taken together, our results show that EGCG is a general inhibitor of NLRP3 inflammasome activation and administration of EGCG in T2D mice could improve glucose tolerance in vivo.

摘要

没食子儿茶素没食子酸酯(EGCG)是绿茶中主要的多酚成分,已被证明能抑制氧化和炎症。然而,EGCG 发挥抗炎作用的确切机制尚不清楚。在这项研究中,我们评估了 EGCG 在体外调节 NLRP3 炎性小体活性的潜在途径。我们发现 EGCG 通过抑制 NLRP3 炎性小体的激活来抑制 caspase-1 的激活和 IL-1β 的分泌在小鼠骨髓来源的巨噬细胞(BMDMs)中。还观察到 EGCG 阻断 NLRP3 介导的 ASC 斑点形成,并减轻 BMDMs 中的细胞焦亡。此外,EGCG 治疗可改善高脂肪饮食(HFD)诱导的葡萄糖耐量,并防止 HFD 诱导的 2 型糖尿病(T2D)小鼠中 NLRP3 炎性小体依赖性炎症。总之,我们的结果表明,EGCG 是 NLRP3 炎性小体激活的通用抑制剂,在 T2D 小鼠中给予 EGCG 可改善体内葡萄糖耐量。

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