南方医科大学学报

南方医科大学学报 ›› 2006, Vol. 26 ›› Issue (09): 1363-1365.

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白黎芦醇对脂多糖诱导大鼠腹腔巨噬细胞活化的抑制作用

马振华； 马清涌； 沙焕臣； 王连才；   

  1. 西安交通大学第一医院肝胆外科； 西安交通大学第一医院肝胆外科 陕西西安710061； 陕西西安710061；
  • 出版日期:2006-09-20 发布日期:2006-09-20

Effect of resveratrol on lipopolysaccharide-induced activation of rat peritoneal macrophages

MA Zhen-hua, MA Qing-yong, SHA Huan-chen, WANG Lian-cai Department of Hepatobiliary Surgery, First Hospital of Xi’an Jiaotong University, Xi’an 710061, China   

  1. 西安交通大学第一医院肝胆外科； 西安交通大学第一医院肝胆外科 陕西西安710061； 陕西西安710061；
  • Online:2006-09-20 Published:2006-09-20

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摘要： 目的探讨脂多糖(LPS)诱导的大鼠腹腔巨噬细胞(PMA)活性变化及白黎芦醇(RESV)对它的抑制作用。方法分离大鼠PMA,随机分为对照组、LPS组和RESVI-V组。培养24h后,分别用免疫组化方法检测核因子-κB(NF-κB)活性,酶联免疫吸附法和硝酸还原法检测细胞上清液中肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)和一氧化氮(NO)水平。结果对照组仅有少量NF-κB的活化。LPS诱导后,PMA出现大量NF-κB的活化,继而细胞上清液中TNF-α、IL-1和NO的水平显著升高。RESV治疗后NF-κB的活性较PMA组逐渐降低,具有剂量依赖性,并且相应的细胞上清液中TNF-α、IL-1和NO水平明显降低。结论RESV可以抑制PMA中NF-κB的活化,从而减少TNF-α、IL-1和NO的过度分泌。 

Abstract: Objective To investigate nuclear factor kappa B (NF-κB) activation induced by lipopolysaccharide (LPS) in rat peritoneal macrophages (PMAs) and the inhibitory effect of resveratrol on NF-κB activation. Methods PMAS from normal SD rats were randomly divided into 7 groups, including a control group, a LPS group and 5 resveratrol groups (I-V). PMAs of the control group were incubated in DMEM, and those in LPS group in DMEM containing LPS (10 μg/ml). PMAS of resveratrol groups I-V were incubated in DMEM containing LPS (10 μg/ml) and different concentrations of resveratrol. After 24 h of incubation, NF-κB activation in the PMAs was determined, and the expression levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1) and nitric oxide (NO) in the culture medium were measured. Results Exposure to LPS resulted in an excessive enhancement of cytokine and NO expressions in the PMAs. Resveratrol at 1.25-10 μg/ml produced a dose- dependent inhibition of cytokine and NO expressions and on NF-κB activation in LPS-stimulated PMAs. Conclusion Resveratrol can inhibit LPS-induced NF-κB activation in rat PMAs and subsequently suppress the expressions of TNF-α, IL-1 and NO. 

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