详细信息
亥茅酚苷对脂多糖诱导巨噬细胞一氧化氮和白介素6表达的影响 被引量:11
Effects of Sec-O-Glucosylhamaudol on expressions of nitric oxide and interleukin-6 in Lipopolysaccharide stimulated murine macrophage
文献类型:期刊文献
中文题名:亥茅酚苷对脂多糖诱导巨噬细胞一氧化氮和白介素6表达的影响
英文题名:Effects of Sec-O-Glucosylhamaudol on expressions of nitric oxide and interleukin-6 in Lipopolysaccharide stimulated murine macrophage
作者:罗超[1];沈立[1];吕昌[2]
机构:[1]绍兴文理学院元培学院;[2]广东省妇幼保健院药学部
年份:2015
卷号:31
期号:11
起止页码:1486
中文期刊名:中国免疫学杂志
外文期刊名:Chinese Journal of Immunology
收录:CSTPCD、、北大核心2014、CSCD2015_2016、北大核心、CSCD
语种:中文
中文关键词:亥茅酚苷;巨噬细胞;炎症;一氧化氮;白介素6
外文关键词:Sec-O-Glucosylhamaudol; Macrophage; Inflammation; Nitric oxide; Interleukin-6
中文摘要:目的:探讨亥茅酚苷对脂多糖(LPS)诱导的小鼠巨噬细胞株RAW264.7炎症介质及细胞因子(NO、IL-6)释放的影响。方法:应用LPS(1μg/ml)刺激RAW264.7细胞,采用不同浓度亥茅酚苷(20、40、80μg/ml)干预,Griess试剂法测定NO释放量;酶联免疫吸附试验(ELISA)测定IL-6释放,用免疫印迹法(Western blot)检测细胞一氧化氮合酶(i NOS)的表达,实时荧光定量反转录聚合酶链反应(RT-PCR)技术分析i NOS、IL-6 mRNA的表达。结果:亥茅酚苷各剂量组(20、40、80μg/ml)均能抑制LPS诱导的RAW264.7细胞NO、IL-6的释放(P<0.01),并下调i NOS蛋白、i NOS mRNA、IL-6 mRNA的表达。结论:亥茅酚苷对LPS诱导的巨噬细胞NO、IL-6释放和i NOS表达有抑制作用,具有一定的抗炎活性。
外文摘要:Objective: To investigate the effect of Sec-O-Glucosylhamaudol on inflammatory mediator and cytokine( NO and IL-6) production in Lipopolysaccharide( LPS) stimulated murine macrophage( RAW264. 7). Methods: Macrophages were induced with LPS,and incubated with different concentrations of Sec-O-Glucosylhamaudol( 20,40,80 μg/ml),the quantity of NO production was measured by Griess reagent; the IL-6 production were measured by enzyme linked immunosorbent assay( ELISA),the expression of nitric oxide synthase( iNOS) in cells were detected by Western blot; the expression of iNOS and IL-6 mRNA were analyzed by real-time PCR. Results: Each concentrations of Sec-O-Glucosylhamaudol( 20,40,80 μg/ml) inhibited the production of NO and IL-6 in LPSstimulated RAW264. 7 cells( P〈0. 01). This compound also reduced the mRNA expression of iNOS and IL-6. Conclusion: Sec-O-Glucosylhamaudol exhibited anti-inflammatory activity by inhibited the NO and IL-6 production in LPS stimulated RAW264. 7 cells.
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