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作 者:刘玮[1] 周红[1] 丁国富[1] 鲁永玲[1] 王良喜[1] 罗平[1]
机构地区:[1]第三军医大学基础部药理学教研室,重庆400038
出 处:《中国临床药理学与治疗学》2005年第3期314-317,共4页Chinese Journal of Clinical Pharmacology and Therapeutics
摘 要:目的:研究CpGODN对细菌脓毒症小鼠的保护作用及其部分作用机制。方法:建立细菌脓毒症小鼠模型,给予不同剂量的CpGODN后,再给予热灭活E .coli攻击小鼠,观察各组小鼠的死亡情况;有效剂量的灭活E .coli攻击小鼠后收集血清,测定血清中TNF α浓度。结果:10mg·kg-1CpGODN预处理小鼠,可缩短灭活E .coli攻击后小鼠的死亡时间;提前给予3d 2mg·kg-1CpGODN ,能提高灭活E .coli攻击小鼠的存活率;CpGODN预处理能有效抑制细胞因子TNF α的释放。结论:适当剂量的CpGODN预处理对灭活E .coli攻击小鼠具有保护作用,其机制可能与抑制Th1型细胞因子TNF α的释放有关。AIM: To investigate the protective effects and mechanisms of CpG ODN on mice with bacterial sepsis. METHODS: The mice with bacterial sepsis were injected with CpG ODN before infected by inactivated Escherichia coli to observe the protective role of CpG ODN. The serum TNF-α was tested. RESULTS: Adequate dosage ( 2.5 mg·kg -1) of CpG ODN protected mice from lethal challenge by inactivated Escherichia coli in a dose and time dependent manner. CpG ODN inhibited the release of TNF-α induced by inactivated Escherichia coli. CONCLUSION: The potent anti-inflammatory effect of CpG ODN on mice with bacterial sepsis. The mechanism may be related to CpG ODN inhibiting the release of TNF-α induced by inactivated Escherichia coli.
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