人参二醇皂苷对失血性休克-内毒素二次打击大鼠肺组织TLR4与IL-18表达的影响  

The effect of panaxadiol saponin on the expressions of TLR4 and IL-18 in lung tissues of rats with acute lung injury induced by hemorrhagic shock-endotoxin two-hit

作　　者：于振香[1] 左孟华[1] 彭丽萍[1] 刘喜春[2] 康劲松[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教研室

出　　处：《中国老年学杂志》2007年第20期1984-1986,共3页Chinese Journal of Gerontology

基　　金：吉林省科委自然科学基金资助(No20030551-3)

摘　　要：目的观察失血性休克复合内毒素二次打击所致急性肺损伤(ALI)大鼠肺组织Toll样受体4(TLR4)及白介素-18(IL-18)表达的变化,探讨TLR4与IL-18在ALI中的作用以及人参二醇皂苷(PDS)和地塞米松(Dex)对其影响。方法利用失血性休克对Wistar大鼠制造第一次打击,之后给予地塞米松(Dex)或人参二醇皂苷(PDS)治疗,再腹腔注入脂多糖(LPS)作为第二次打击。二次打击6h后处死动物,取肺组织,通过RT-PCR检测TLR4和IL-18 mRNA,通过Western blot检测IL-18蛋白的表达。结果与假手术对照组相比,二次打击可使肺组织TLR4 mRNA、IL-18 mR-NA及IL-18蛋白表达水平明显升高(均P<0.01),而Dex或PDS预治疗则能显著降低其含量(P<0.05)。结论失血性休克-内毒素二次打击所致急性肺损伤可能通过增加TLR4功能从而使其介导的信号转导作用加强,导致IL-18等炎症介质的分泌增加引起肺损伤,而PDS通过抑制TLR4介导的信号转导通路,减少IL-18等炎性介质的释放从而减轻肺损伤。Objective To observe the changes in the expressions of Toll like receptor （TLR） 4 and IL-18 in lung tissues of acute lung injury （ALI） induced by hemorrhage-LPS two-hit to investigate the effect of TLR4 and IL-18 in ALI and the effects of dexamethasone and panaxadiol saponins （PDS）. Methods Forty Wistar rats were divided randomly into sham operational group, two-hit group with hemorrhage-lipopolysaccharides （HL group）, dexamethasone preventive therapy, PDS preventive therapy groups. The rats with first-hit by hemorrhagic shock were treated dexamethasone and panaxadiol saponins, then injected intraperitoneally lipopolysaccharide （LPS） as the second hit. The rats were killed 6 h after two-hit to obtain lung tissue to determine TLR4 and IL-18 mRNA expressions by RT-PCR and IL-18 protein expression by Western blot. Results TLR4 and IL-18 mRNA and IL-18 protein expressions in lung tissue after two-hit were higher than those in sham operation group （ all P 〈0.01 ） , but were obviously reduced by dexamethasone and PDS injections （ P 〈 0. 05 ）. Conclusions The mechanism of ALI induced by hemorthage-LPS two-hit is to increase the mediators of inflammation secretion, such as IL-8 etc. through enhancing TLR4 function to promote the induced signal transduction. PDS injection could block the TLR4 induced signal transduction pathway and decrease the expressions of the IL-18 to lessen the lung damage.

关 键 词：急性肺损伤 二次打击 人参二醇皂苷 TOLL样受体4 白介素18 

分 类 号：R-363[医药卫生] R605.971