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首页> 外文期刊>The Journal of Nutritional Biochemistry >Epigallocatechin-3-gallate suppresses NF- kappa B activation and phosphorylation of p38 MAPK and JNK in human astrocytoma U373MG cells.
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Epigallocatechin-3-gallate suppresses NF- kappa B activation and phosphorylation of p38 MAPK and JNK in human astrocytoma U373MG cells.

机译：Epigallocatechin-3-gallate抑制人星形细胞瘤U373MG细胞中NF-κB的活化以及p38 MAPK和JNK的磷酸化。

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摘要

Epigallocatechin-3-gallate (EGCG) is the major polyphenol component of green tea and is primarily responsible for the green tea effect. EGCG possesses two triphenolic groups in its structure. These groups are reported to be important with respect to anticarcinogenic and antioxidant effects. However, the anti-inflammatory effect of EGCG on Alzheimer's disease (AD) is still not fully understood. In this study, we investigated the effects of EGCG in attenuating the inflammatory response induced by interleukin (IL)-1 beta + beta -amyloid (25-35) fragment (A beta ) in human astrocytoma, U373MG cells. EGCG significantly inhibited the IL-1 beta +A beta (25-35)-induced IL-6, IL-8, vascular endothelial growth factor (VEGF) and prostaglandin (PG)E< sub>2 production at 24 h (P<.01). The maximal inhibition rate of IL-6, IL-8, VEGF and PGE< sub>2 production by EGCG was approximately 54.40%, 56.01%, 69.06% and 47.03%, respectively. EGCG also attenuated the expression of cyclooxygenase-2 and activation of nuclear factor- kappa B induced by IL-1 beta +A beta (25-35). We demonstrated that EGCG suppresses IL-1 beta +A beta (25-35)-induced phosphorylation of the mitogen-activated protein kinase p38 and the c-Jun N-terminal kinase. In addition, EGCG induced the expression of mitogen-activated protein kinase phosphatase-1. These results provide new insight into the pharmacological actions of EGCG and its potential therapeutic application to various neurodegenerative diseases such as AD.
机译：Epigallocatechin-3-gallate（EGCG）是绿茶中的主要多酚成分，主要负责绿茶的功效。 EGCG在其结构上具有两个三酚基团。据报道这些组在抗癌和抗氧化作用方面很重要。但是，EGCG对阿尔茨海默氏病（AD）的抗炎作用仍未完全了解。在这项研究中，我们研究了EGCG在减轻人星形细胞瘤U373MG细胞中由白介素（IL）-1β+β淀粉样蛋白（25-35）片段（A beta）诱导的炎症反应中的作用。 EGCG在24岁时显着抑制IL-1 beta + A beta（25-35）诱导的IL-6，IL-8，血管内皮生长因子（VEGF）和前列腺素（PG）E 2 的产生h（P <.01）。 EGCG对IL-6，IL-8，VEGF和PGE 2 产生的最大抑制率分别约为54.40％，56.01％，69.06％和47.03％。 EGCG还减弱了IL-1 beta + A beta诱导的环氧合酶2的表达和核因子-κB的激活（25-35）。我们证明了EGCG抑制IL-1 beta + A beta（25-35）诱导的丝裂原活化蛋白激酶p38和c-Jun N端激酶的磷酸化。此外，EGCG诱导有丝分裂原激活的蛋白激酶磷酸酶-1的表达。这些结果为EGCG的药理作用及其对各种神经退行性疾病（如AD）的潜在治疗应用提供了新的见解。

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