摘要
目的 :观察地塞米松 (Dex)和白细胞介素 (IL) - 1 0对培养的经脂多糖 (LPS)刺激的人外周血单个核细胞 (hPBMC)释放促炎细胞因子肿瘤坏死因子 (TNF) -α、IL - 6及对转录因子核因子 -κB(NF -κB)、活化蛋白 - 1(AP - 1 )、cAMP反应元件结合蛋白 (CREB)活化的影响。方法 :用LPS刺激分离培养的hPBMC ,分为正常对照组、LPS刺激组、IL - 1 0和Dex干预组。ELISA法检测培养上清中TNF -α、IL - 6含量。凝胶电泳迁移率改变分析法 (EMSA)检测核提取物中NF -κB、AP - 1、CREB活性。结果 :LPS刺激 1h后TNF -α含量显著增加 ,Dex和IL - 1 0干预后TNF-α含量增加被显著抑制 ;IL - 6含量在LPS刺激后 1 2h显著增加 ,Dex和IL - 1 0显著抑制IL - 6的产生 ;LPS刺激 1 2h后IL - 1 0含量显著增加 ,Dex对IL - 1 0产生没有明显影响。LPS刺激 1h后NF -κB、AP - 1、CREB的DNA结合活性显著增加 ,Dex和IL - 1 0显著抑制以上三种核因子的活性 ,但Dex对AP - 1、CREB活性的抑制作用强于IL - 1 0。结论 :LPS诱导hPBMC释放多种促炎和抗炎细胞因子的产生 ,并诱导多种转录因子的活化 ;Dex、IL - 1 0能抑制上述促炎细胞因子的产生和转录因子的活化。Dex对AP - 1、CREB活性的抑制作用强于IL - 1 0。
AIM: To observe the effects of dexamethasone and interleukin-10 (IL-10) on the release of proinflammatory cytokines, tumor necrosis factor-α(TNF-α), IL-6 and activation of transcriptional factors, nuclear factor-κB(NF-κB), activator protein-1 (AP-1) and cAMP response element binding protein (CREB) in cultrued human peripheral blood mononuclear cells (hPBMC). METHODS: The hPBMC were divided into control group, lipopolysaccharide (LPS) stimulated group, dexamethasone and IL-10 treated group. The contents of TNF-α and IL-6 in supernatant were mensured by ELISA. The activity of NF-κB, AP-1 and CREB of nuclear abstract were analyzed by electrophoretic morbility shift assay (EMSA). RESULTS: The content of TNF-α was significantly increased 1 hour after LPS stimulation, and it was significantly inhibition by dexamethasone and IL-10. The contents of IL-6 and IL-10 were significantly increased after LPS stimulation for 12 hours. The production of IL-6 was still inhibited by dexamethasone and IL-10, but the production of IL-10 was not affected by dexamethasone. The activities of NF-κB, AP-1 and CREB were significantly increased 1 hour after LPS stimulation. Dexamethasone and IL-10 significantly ihibited their activities, but the effects of dexamethasone was stronger than that of IL-10. CONCLUSIONS: LPS induces the release of several pro and anti- inflammatory cytokines and induces the activation of several transcriptional factors in hPBMC. Dexamethasone and IL-10 can inhibite the production of proinflammatory cytokines TNF-α, IL-6 and the activation of NF-κB, AP-1 and CREB. Dexamthasone has more significant inhibitory effect on AP-1 and CREB than IL-10.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第11期1328-1332,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金重点资助项目 (No .39730 2 1 0 )
