Green tea polyphenol epigallocatechin-3-gallate inhibits the IL-1β-induced activity and expression of cyclooxygenase-2 and nitric oxide synthase-2 in human chondrocytes
Green tea polyphenol epigallocatechin-3-gallate inhibits the IL-1β-induced activity and expression of cyclooxygenase-2 and nitric oxide synthase-2 in human chondrocytes
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DOI：
10.1016/s0891-5849(02)01004-3
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发表时间：
2002-10-15
影响因子：
7.4
通讯作者：
Haqqi, TM
中科院分区：
文献类型：
--
作者：
Ahmed, S;Rahman, A;Haqqi, TM
我们先前已经证明，绿色茶多酚抑制小鼠II型胶原诱导的关节炎的发作和严重程度。在本研究中，我们报告了绿色茶多酚表没食子儿茶素没食子酸酯（EGCG）的药理作用，对白细胞介素-1 β（IL-1 β）诱导的表达和活性的环氧合酶-2（考克斯-2）和诱导型一氧化氮合酶（iNOS）的人软骨细胞从骨关节炎（OA）软骨。用IL-1 β（5 ng/ml）刺激人软骨细胞24小时，与未处理的对照组相比，它导致一氧化氮（NO）和前列腺素E-2（PGE（2））的产生显著增加（p <0.001）。用表没食子儿茶素没食子酸酯（EGCG）预处理人软骨细胞显示出对NO和PGE（2）产生的剂量依赖性抑制，分别为48%和24%，并且与iNOS和考克斯-2活性的抑制相关（p <0.005）。此外，在用EGCG预处理的人软骨细胞中，IL-1 β诱导的iNOS和考克斯-2的表达也被显著抑制（p <0.001）。与这些发现平行，EGCG也抑制软骨细胞培养中IL-1 β诱导的LDH释放。总的来说，这项研究表明，EGCG通过调节各自酶的表达和催化活性，对IL-1 β诱导的人软骨细胞中分解代谢介质NO和PGE（2）的产生提供保护。此外，我们的研究结果还表明，ECGC可能具有潜在的治疗价值，抑制关节炎关节软骨吸收。(C)2002年爱思唯尔科技有限公司
We have previously shown that green tea polyphenols inhibit the onset and severity of collagen II-induced arthritis in mice. In the present study, we report the pharmacological effects of green tea polyphenol epigallocatechin-3-gallate (EGCG), on interleukin-1beta (IL-1beta)-induced expression and activity of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in human chondrocytes derived from osteoarthritis (OA) cartilage. Stimulation of human chondrocytes with IL-1beta (5 ng/ml) for 24 It resulted in significantly enhanced production of nitric oxide (NO) and prostaglandin E-2 (PGE(2)) when compared to untreated controls (p < .001). Pretreament of human chondrocytes with EGCG showed a dose-dependent inhibition in the production of NO and PGE(2) by 48% and 24%, respectively, and correlated with the inhibition of iNOS and COX-2 activities (p < .005). In addition, IL-1beta-induced expression of iNOS and COX-2 was also markedly inhibited in human chondrocytes pretreated with EGCG (p < .001). Parallel to these findings, EGCG also inhibited the IL-1beta-induced LDH release in chondrocytes cultures. Overall, the study suggests that EGCG affords protection against IL-1beta-induced production of catabolic mediators NO and PGE(2) in human chondrocytes by regulating the expression and catalytic activity of their respective enzymes. Furthermore, our results also indicate that ECGC may be of potential therapeutic value for inhibiting cartilage resorption in arthritic joints. (C) 2002 Elsevier Science Inc.