蟛蜞菊内酯对脂多糖诱导RAW264.7细胞环氧化酶2、NO及TNF-α的影响

中国临床药理学与治疗学 ›› 2012, Vol. 17 ›› Issue (2): 171-174.

蟛蜞菊内酯对脂多糖诱导RAW264.7细胞环氧化酶2、NO及TNF-α的影响

陈杰¹, 李瑞明¹, 许静², 官碧琼², 罗子玲²

¹中山大学附属第一医院药学部,广州 510008,广东;
²南方医科大学第三附属医院药剂科, 广州 510630, 广东

收稿日期:2011-12-07 修回日期:2012-01-17 出版日期:2012-02-26 发布日期:2012-03-12
通讯作者: 许静,主管药师,主要从事临床药学工作。E-mail: hsujing77@163.com
作者简介:陈杰,主管药师,主要从事临床药学工作。E-mail: chenjiezs@163.com
基金资助:
广东省自然科学基金(8451008901000788);广东省医学科研基金(A2009163)

Effect of Wedelolactone on COX-2, NO and TNF-α expression in lipopolysaccharide induced RAW264.7 cells

CHEN Jie¹, LI Rui-ming¹, XU Jing², GUAN Bi-qiong², LUO Zi-ling²

¹Department of Pharmacy, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China;
²Department of Pharmacy, the Third Affiliated Hospital , Southern Medical University, Guangzhou 510630, Guangdong, China

Received:2011-12-07 Revised:2012-01-17 Online:2012-02-26 Published:2012-03-12

摘要/Abstract

摘要： 目的: 研究蟛蜞菊内酯对脂多糖(lipopolysaccharide,LPS)诱导RAW264.7巨噬细胞环氧化酶2(COX-2)、NO及TNF-α的作用。方法: ELISA方法检测 0.2、2、20 μmol/L 不同浓度蟛蜞菊内酯对终浓度为10 μg/mL LPS诱导RAW264.7细胞产生TNF-α、NO及前列腺素E₂(PGE₂)的影响,Western blot方法检测蟛蜞菊内酯对LPS诱导COX-2 酶蛋白表达的影响。结果: LPS能够明显诱导小鼠RAW264.7细胞产生的COX-2酶蛋白,蟛蜞菊内酯低中高3个浓度均能抑制LPS诱导产生的COX-2酶蛋白表达。PGE₂可以被 LPS诱导增加,与空白组比有显著差异。蟛蜞菊内酯低中高3个浓度均能抑制LPS诱导产生的PGE₂、NO和TNF-α,呈现剂量依赖性。结论: 蟛蜞菊内酯抗炎的作用机制可能为抑制COX-2的蛋白表达,进而抑制PGE₂的生成,也可能与抑制NO和TNF-α生成有关。

关键词: 蟛蜞菊内酯, 脂多糖, 细胞培养

Abstract: AIM: To study effect of Wedelolactone on COX-2, NO and TNF-α expression in lipopolysaccharide (LPS) induced RAW264.7 cells.METHODS: The contents of PGE₂, TNF-α, NO were detected by ELISA methods, expression of COX-2 protein in RAW264.7 cells was measured by MTT assay, in the presence or absence of 10 μg/mL lipopolysaccharide (LPS) or Wedelolactone (0.2, 2, 20 μmol/L).RESULTS: The expression of COX-2 protein was significantly induced by LPS, Wedelolactone inhibited the expression of COX-2 protein significantly elicited by LPS in RAW264.7 cells; LPS-induced PGE₂, TNF-α, NO was significantly inhibited by Wedelolactone in RAW264.7 cells, in dose dependent manners.CONCLUSION: The anti-inflammatory mechanisms of TGA may suppress production of PGE₂ through inhibiting COX-2 gene expression, and inhibit activity of NO and TNF-α.

Key words: Wedelolactone, Lipopolysaccharide, Cell culture

中图分类号:

R965.2

陈杰, 李瑞明, 许静, 官碧琼, 罗子玲. 蟛蜞菊内酯对脂多糖诱导RAW264.7细胞环氧化酶2、NO及TNF-α的影响[J]. 中国临床药理学与治疗学, 2012, 17(2): 171-174.

CHEN Jie, LI Rui-ming, XU Jing, GUAN Bi-qiong, LUO Zi-ling. Effect of Wedelolactone on COX-2, NO and TNF-α expression in lipopolysaccharide induced RAW264.7 cells[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2012, 17(2): 171-174.

参考文献

[1] Kobori M, Yang Z, Gong D, et al. Wedelolactone suppresses LPS-induced caspase-11 expression by directly inhibiting the IKK complex[J]. Cell Death Differ, 2004, 11(1):123-130.
[2] Melo PA, do Nascimento MC, Mors WB, et al. Inhibition of the myotoxic and hemorrhagic activities of crotalid venoms by Eclipta prostrata (Asteraceae) extracts and constituents[J]. Toxicon, 1994, 32(5): 595-603.
[3] Jayathirtha MG, Mishra SH. Preliminary immunomodulatory activities of methanol extracts of Eclipta alba and Centella asiatica[J]. Phytomedicine, 2004, 11(4): 361-365.
[4] Wagner H, Geyer B, Kiso Y, et al. Coumestans as the main active principles of the liver drugs Eclipta alba and Wedelia calendulacea[J]. Planta Med, 1986, 5(1): 370-374.
[5] 严梅娣, 叶孟, 林蕾, 等. 槲寄生凝集素腹腔内给药对腹腔巨噬细胞功能的影响[J]. 中国临床药理学与治疗学, 2010(2): 126-129.
[6] 周国勇, 胡森, 吕艺, 等. 卡巴胆碱对内毒素刺激大鼠腹腔巨噬细胞炎症细胞因子表达的影响[J]. 中国临床药理学与治疗学, 2009(12): 1361-1365.
[7] Ho FM, Lai CC, Huang LJ, et al. The anti-inflammatory carbazole, LCY-2-CHO, inhibits lipopolysaccharide-induced inflammatory mediator expression through inhibition of the p38 mitogen-activated protein kinase signaling pathway in macrophages[J]. Br J Pharmacology, 2004, 141(6): 1037-1047.
[8] Lee AK, Sung SH, Kim YC, et al. Inhibition of lipopolysaccharide-inducible nitric oxide synthase, TNF-α and COX-2 expression by sauchinone effects on I-κBα phosphorylation, C/EBP and AP-1 activation[J]. Br J Pharmacol, 2003, 139(1): 11-20.
[9] Takayukl N, Norlko M, Glovanna T, et al. Prostaglandin E2 promotes degranulation-independent release of MCP-1 from mast cells[J]. J Leukoc Biol, 2006, 79(1):1-10.
[10] Xiao C, Li J, Dong X, et al. Anti-oxidative and TNF-alpha suppressive activities of puerarin derivative (4AC) in RAW264.7 cells and collagen-induced arthritic rats[J]. Eur J Pharmacol, 2011, 666(1/2/3): 242-250.

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