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作 者:吴学玲[1] 钱桂生[1] 徐德斌[1] 侯一峰[1]
机构地区:[1]第三军医大学新桥医院全军呼吸病研究所,重庆400037
出 处:《中国急救医学》2005年第1期46-48,共3页Chinese Journal of Critical Care Medicine
基 金:国家自然科学基金资助课题 (No .3 0 170 3 66)
摘 要:目的 研究脂多糖结合蛋白 (LBP)抑制肽对内毒素 (LPS)诱导的人单核巨噬细胞株U937细胞TLR4的影响。方法 佛波脂 (PMA)诱导U937成熟后分为 5组 ,即正常对照组 ;LPS组 ;低剂量抑制肽组 ;中剂量抑制肽组 ;高剂量抑制肽组。用RT-PCR和蛋白定量方法 (Westernblot)测定TLR4mRNA和蛋白的表达 ,ELISA测定培养上清液中肿瘤坏死因子 -α(TNF -α)的含量。结果 LBP抑制肽组TLR4的mRNA ,蛋白的OD值 ,TNF -α的浓度均较LPS组低 ,较正常组高。结论 LBP抑制肽通过抑制由TLR4介导的LPS信号跨膜转导和TNF -α的分泌 ,对LPS所致疾病如脓毒血症、急性肺损伤可能有潜在的治疗作用。Objective To investigate the effects of LBP inhibitory peptide on TLR4 of U937 induced by LPS.Methods U937 was stimulated by phorbol-myritate-acetate( PMA 100 ng/mL) and divided into five groups: control group;LPS group(10 ng/mL LPS+100 ng/mL rhLBP);low dose inhibitory peptide group; middle dose inhibitory peptide group; high dose inhibitory peptide group (10 ng/mL,100 ng/mL and 1 000 ng/mL inhibitory peptide respectively ). The mRNA and protein of CD 14was determined by RT-PCR and Western blot and the concentration of TNFα released from U937 was detected by ELISA.Results Optical density(OD) of TLR4 mRNA and protein in inhibitory peptide group was lower than that in LPS group and higher than that in control group.The concentration of TNFα in inhibitory peptide group was lower than that in LPS group and higher than that in control group.Conclusion LBP inhibitory peptide might have a potential protective role in LPS induced inflammation such as sepsis and acute lung injury by inhibiting the mRNA and protein expression of TLR4 and reducing the release of TNFα.
关 键 词:脂多糖结合蛋白抑制肽 脂多糖 CD14 肿瘤坏死因子-Α
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