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芍药总苷对大鼠胶原诱导性关节炎滑膜细胞活性的影响及机制

Effects and mechanisms of total glucosides of paeony on synoviocytes activities in rat collagen-induced arthritis.

作者信息

Chang Yan, Wei Wei, Zhang Lei, Xu Hong-Mei

机构信息

Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immunopharmacology in Anhui Province, Hefei 230032, Anhui Province, China.

出版信息

J Ethnopharmacol. 2009 Jan 12;121(1):43-8. doi: 10.1016/j.jep.2008.09.028. Epub 2008 Oct 7.

DOI:10.1016/j.jep.2008.09.028
PMID:18977427
Abstract

The aim of the study was to investigate the effects of TGP, an active compound extracted from the roots of Paeonia lactiflora Pall, on the activities of synoviocytes in rats with collagen-induced arthritis (CIA) and its possible mechanisms. CIA was induced in male Sprague-Dawley (SD) rats immunized with chicken type II collagen (CII) in Freund's complete adjuvant (FCA). Synoviocytes proliferation was determined by 3-(4, 5-2dimethylthiazal-2yl) 2, 5-diphenyltetrazoliumbromide (MTT) assay. Tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP) levels in synoviocytes were measured by radioimmunoassay (RIA). E-prostanoid (EP)(2) and EP(4) receptors were analyzed by Western blot analysis. The results showed that TGP significantly inhibited the proliferation of synoviocytes, decreased the production of IL-1, TNF-alpha and PGE(2) and elevated the levels of cAMP. Further study showed that TGP could up-regulate the expression of EP(2) and EP(4). These results indicated that TGP might exert its anti-inflammatory effects through inhibiting the production of pro-inflammatory mediators in synoviocytes of CIA rats, which might be associated with its ability to regulate cAMP-dependent EP(2)/EP(4)-mediated pathway.

摘要

本研究旨在探讨从芍药根中提取的活性化合物白芍总苷(TGP)对胶原诱导性关节炎(CIA)大鼠滑膜细胞活性的影响及其可能机制。采用鸡Ⅱ型胶原(CII)与弗氏完全佐剂(FCA)免疫雄性Sprague-Dawley(SD)大鼠诱导CIA。采用3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐(MTT)法检测滑膜细胞增殖。采用放射免疫分析法(RIA)检测滑膜细胞中肿瘤坏死因子α(TNF-α)、白细胞介素-1(IL-1)、前列腺素E2(PGE2)和环磷酸腺苷(cAMP)水平。通过蛋白质印迹分析检测E-前列腺素(EP)2和EP4受体。结果显示,TGP显著抑制滑膜细胞增殖,降低IL-1、TNF-α和PGE2的产生,并提高cAMP水平。进一步研究表明,TGP可上调EP2和EP4的表达。这些结果表明,TGP可能通过抑制CIA大鼠滑膜细胞中促炎介质的产生发挥抗炎作用,这可能与其调节cAMP依赖的EP2/EP4介导途径的能力有关。

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