摘要
目的:研究蟛蜞菊内酯对脂多糖(lipopo-lysaccharide,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、20μmol/L不同浓度蟛蜞菊内酯对终浓度为10μg/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。
AIM： To study effect of Wedelo- lactone on COX-2, NO and TNF-α expression in lipopolysaccharide （LPS） induced RAW2G4. 7 cells. METHODS： The contents of PGE2, TNF- α, NO were detected hy ELISA methods, expression of COX-2 protein in RAW2G4. 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 in- hibited 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 .
出处
《中国临床药理学与治疗学》
CAS
CSCD
2012年第2期171-174,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
广东省自然科学基金(8451008901000788)
广东省医学科研基金(A2009163)
关键词
蟛蜞菊内酯
脂多糖
细胞培养
Wedelolactone
Lipopolysaccha- ride
Cell culture
