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绿茶和表没食子儿茶素没食子酸酯在脂多糖诱导的全身炎症模型中的保护作用。

Protective effect of green tea and epigallocatechin-3-gallate in a LPS-induced systemic inflammation model.

机构信息

Hematology and Transfusion Medicine Center, University of Campinas, Campinas, São Paulo, Brazil.

Hematology and Transfusion Medicine Center, University of Campinas, Campinas, São Paulo, Brazil.

出版信息

J Nutr Biochem. 2022 Mar;101:108920. doi: 10.1016/j.jnutbio.2021.108920. Epub 2021 Dec 4.

DOI:10.1016/j.jnutbio.2021.108920
PMID:34875388
Abstract

Inflammation causes severe dysregulation of organ functions, via the development of oxidative stress and inflammation damage. Polyphenol compounds found in green tea (GTE), including the most important component epigallocatechin-3-gallate (EGCG), have a great therapeutic potential. Here, protective properties of GTE and EGCG against lipopolysaccharide (LPS)-induced inflammation are explored. To this end, the effects of GTE and EGCG were studied on LPS challenged macrophages. Mice received GTE (250 mg/kg/d/p.o) or EGCG (25 mg/kg/d/i.p.) for 7 d, before the inflammation shock was provoked with a single intraperitoneal injection of LPS. The frequencies of lymphocytes CD4, CD8, NK1-1 and CD4CD25FOXP3 (Treg), macrophages CD11bF480, monocytes CD11bLy6C, neutrophils CD11bLy6G, MDSCs CD11bGr-1, M2/N2-like phenotype CD206 and M1-like phenotype CD86 in spleen, bone marrow and peripheral blood were determined. In vitro studies revealed that GTE and EGCG significantly attenuated LPS-induced CD80 expression and increased the CD163 expression, showing a potential to reduce the macrophage inflammatory phenotype. In vivo, GTE and EGCG inhibited the inflammation, mainly by reducing M1-macrophages and increasing Treg cells in the bone marrow. In addition, GTE and EGCG increase M2-macrophages, N2-neutrophils and Tregs in the spleen and blood and block the migration of monocytes from the bone marrow to the peripheral blood. These findings indicate that EGCG and GTE prevent LPS-induced inflammatory damage contributing to restoring the immune system homeostasis.

摘要

炎症通过氧化应激和炎症损伤导致器官功能严重失调。绿茶(GTE)中发现的多酚化合物,包括最重要的成分表没食子儿茶素-3-没食子酸酯(EGCG),具有巨大的治疗潜力。在这里,研究了 GTE 和 EGCG 对脂多糖(LPS)诱导的炎症的保护作用。为此,研究了 GTE 和 EGCG 对 LPS 挑战的巨噬细胞的影响。在炎症休克之前,用 LPS 单次腹腔注射,给小鼠口服 GTE(250mg/kg/d/p.o)或 EGCG(25mg/kg/d/i.p.)7 天。用流式细胞术测定脾、骨髓和外周血中淋巴细胞 CD4、CD8、NK1-1 和 CD4CD25FOXP3(Treg)、巨噬细胞 CD11bF480、单核细胞 CD11bLy6C、中性粒细胞 CD11bLy6G、MDSC CD11bGr-1、M2/N2 样表型 CD206 和 M1 样表型 CD86 的频率。体外研究表明,GTE 和 EGCG 显著减弱 LPS 诱导的 CD80 表达,增加 CD163 表达,具有减少巨噬细胞炎症表型的潜力。在体内,GTE 和 EGCG 抑制炎症,主要是通过减少骨髓中的 M1 巨噬细胞和增加 Treg 细胞。此外,GTE 和 EGCG 增加脾和血液中的 M2 巨噬细胞、N2 中性粒细胞和 Tregs,并阻止单核细胞从骨髓向外周血的迁移。这些发现表明,EGCG 和 GTE 可预防 LPS 诱导的炎症损伤,有助于恢复免疫系统的稳态。

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