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没食子单宁通过 ERK-1/2 和 p38 激酶通路诱导兔关节软骨细胞分化和炎症反应。

Gallotannin causes differentiation and inflammation via ERK‑1/‑2 and p38 kinase pathways in rabbit articular chondrocytes.

机构信息

Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongju, Chungnam 314‑701, Republic of Korea.

出版信息

Mol Med Rep. 2013 Feb;7(2):701-7. doi: 10.3892/mmr.2012.1204. Epub 2012 Nov 27.

DOI:10.3892/mmr.2012.1204
PMID:23229854
Abstract

Gallotannin (GT) is a type of tannic acid, derived from plant polyphenols, that is an agonist of plant defense mechanisms. Tannins have two types of structure; condensed tannins are a polymer of flavonoid units, while hydrolysable tannins are carbohydrates. GT is used in medical agents for its anti‑viral, anti‑bacterial and anti‑parasitic effects. The present study investigated the effects of GT on differentiation and inflammation in rabbit articular chondrocytes. GT caused differentiation and inflammatory responses in the rabbit articular chondrocytes. GT treatment induced the expression of type Ⅱ collagen and sulfated proteoglycan, as determined by western blot analysis and alcian blue staining, respectively, in a dose‑ and time‑dependent manner. Additionally, treatment with GT increased the expression of cyclooxygenase‑2 (COX‑2) and the production of prostaglandin E2 (PGE2), as determined by western blot analysis and PGE2 assay. GT was confirmed to cause phosphorylation of ERK‑1/‑2 and p38 kinase. Inhibition of pERK with PD98059 promoted GT‑induced type Ⅱ collagen expression. However, the inhibition of p38 with SB203580 suppressed GT‑induced COX‑2 expression and PGE2 production. In summary, the results demonstrated that GT‑induced ERK‑1/‑2 and p38 kinase have opposite effects on differentiation and inflammation in rabbit articular chondrocytes.

摘要

没食子单宁(GT)是一种植物多酚衍生的鞣酸,是植物防御机制的激动剂。单宁有两种结构类型;缩合单宁是类黄酮单元的聚合物,而可水解单宁是碳水化合物。GT 因其抗病毒、抗菌和抗寄生虫作用而被用于医学制剂。本研究探讨了 GT 对兔关节软骨细胞分化和炎症的影响。GT 导致兔关节软骨细胞发生分化和炎症反应。通过 Western blot 分析和阿尔辛蓝染色分别确定,GT 以剂量和时间依赖的方式诱导 II 型胶原和硫酸软骨素蛋白聚糖的表达。此外,通过 Western blot 分析和 PGE2 测定,GT 处理增加了环氧化酶-2(COX-2)的表达和前列腺素 E2(PGE2)的产生。GT 被证实可引起 ERK-1/-2 和 p38 激酶的磷酸化。用 PD98059 抑制 pERK 促进 GT 诱导的 II 型胶原表达。然而,用 SB203580 抑制 p38 抑制了 GT 诱导的 COX-2 表达和 PGE2 产生。总之,研究结果表明,GT 诱导的 ERK-1/-2 和 p38 激酶对兔关节软骨细胞的分化和炎症有相反的影响。

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