人参二醇皂苷对失血-内毒素二次打击模型大鼠肿瘤坏死因子α和白细胞介素6含量的影响  

Effects of panaxadiol saponins on contents of TNF-α and IL-6 in two-hit rat models with hemorrhage and lipopolysaech

作　　者：于振香[1] 丁艳华[1] 李璐[2] 赵雪俭[2] 

机构地区：[1]吉林大学第一医院呼吸内科,吉林长春130021 [2]吉林大学基础医学院病理生理学教研室,吉林长春130021

出　　处：《吉林大学学报（医学版）》2005年第6期890-892,共3页Journal of Jilin University：Medicine Edition

基　　金：吉林省科技厅自然科学基金资助课题(20030551-3)

摘　　要：目的:探讨失血-内毒素二次打击模型大鼠血清中肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)含量的变化,以及人参二醇皂苷(PDS)对其影响。方法:Wistar大鼠随机分为假手术对照组(S组)、失血性休克组(H组)、失血-内毒素双打击组(HL组)、地塞米松预治疗组(HLD组)及PDS预治疗组(HLP组)。在失血性休克首次打击的基础上,用内毒素作为第二次打击复制大鼠难治性休克模型,6 h后处死动物,用放射免疫分析法测定血清TNF-α和IL-6的含量。结果:血清TNF-α和IL-6含量,H组、HL组与S组比较均明显升高,但以HL组尤为明显(P<0.01,P<0.001),而HLP组和HLD组的TNF-α含量和IL-6含量则明显地低于HL组(均P<0.01)。结论:在失血性休克基础上给予内毒素可显著地提高TNF-α和IL-6的血清水平;PDS和地塞米松有类似的抑制TNF-α和IL-6的释放,保护失血-内毒素二次打击大鼠的作用。Objective To explore the changes of serum TNF-α and IL-6 contents in the two-hit rat models with hemorrhage and lipopolysaech （LPS） and the effects of panaxadiol saponins （PDS） on TNF-α and contents IL-6. Methods Adult Wistar rats were randomly divided into 5 groups： sham operational group （S）, hemorrhage group （H）, two-hit group with hemorrhage and LPS groups （HL）, Dexamethasone pretreatment group （HLD）, PDS pretreatment group （HLP）. The rat models were made by hemorrhagic shock as the first hit and with endotoxin as the second hit. Then the rats were killed after 6 h. The contents of serum TNF-α and IL-6 in rats were measured by radioimmunoassay. Results The serum TNF-α and IL-6 contents in HL group were increased significantly compared with S group or H group （P〈0. 001）. The TNF-α and IL-6 contents in HLP group and HLD group were significantly lower than those in HL group （P〈0. 01）. Conclusion LPS can increase significantly the contents of serum TNF-α and IL-6 in rats with hemorrhagic shock. PDS can inhibit the release of serum TNF-α and IL-6, and has the same effects with DEX to protect against the tissue injuries of two-hit rats with hemorrhage and LPS.

关 键 词：失血-内毒素二次打击大鼠 休克 人参二醇 肿瘤坏死因子 白细胞介素6 模型 动物 

分 类 号：R-332[医药卫生] R605.971