CAJ | 학술논문

目的：应用地塞米松( dexamethasone,Dex)干预小鼠内毒素耐受的形成,研究糖皮质激素对内毒素耐受的影响。方法以昆明鼠为实验对象进行分组,ⅠA组为健康对照组,ⅠB组为单次直接致死剂量脂多糖(lipopolysaccharide,LPS)(2LD50=8 mg/kg)对照组,Ⅱ组为标准内毒素耐受组,ⅢA组为初始LPS刺激前高剂量Dex(10 mg/kg)干预组,ⅢB组为终末致死量 LPS 前高剂量 Dex 干预组,ⅣA 组为初始 LPS 刺激前低剂量Dex(1 mg/kg)干预组,ⅣB组为终末致死量 LPS 前低剂量 Dex 干预组。完成实验处置后3 h 取血标本,应用ELISA方法检测血清TNF-α和IL-10水平。结果①ⅠA组TNF-α、IL-10水平极低,ⅠB组TNF-α、IL-10水平较ⅠA组显著增高(P<0．05,P<0．01),Ⅱ组TNF-α、IL-10水平较ⅠB组显著下降(P<0．05,P<0．01),但仍高于ⅠA组。②各Dex干预组TNF-α水平与Ⅱ组比较：ⅢA、ⅣA组TNF-α水平与Ⅱ组TNF-α水平差异无统计学意义(P>0．05),ⅢB、ⅣB组TNF-α水平低于Ⅱ组,差异有统计学意义(P<0．05)。③各Dex干预组IL-10水平与Ⅱ组比较：ⅢA、ⅣA组IL-10水平高于Ⅱ组,差异有统计学意义(P<0．05),ⅢB、ⅣB组IL-10水平与Ⅱ组比较差异无统计学意义(P>0．05)。结论①LPS刺激可导致小鼠体内 TNF-α水平、IL-10水平升高。内毒素耐受时,小鼠体内TNF-α、IL-10水平升高的程度明显降低。②终末LPS前一定时间内予以Dex干预可以促进内毒素耐受的形成,Dex剂量过高可能不会带来更多受益。③IL-10对内毒素耐受的形成可能不具有决定作用。
목적：응용지새미송( dexamethasone,Dex)간예소서내독소내수적형성,연구당피질격소대내독소내수적영향。방법이곤명서위실험대상진행분조,ⅠA조위건강대조조,ⅠB조위단차직접치사제량지다당(lipopolysaccharide,LPS)(2LD50=8 mg/kg)대조조,Ⅱ조위표준내독소내수조,ⅢA조위초시LPS자격전고제량Dex(10 mg/kg)간예조,ⅢB조위종말치사량 LPS 전고제량 Dex 간예조,ⅣA 조위초시 LPS 자격전저제량Dex(1 mg/kg)간예조,ⅣB조위종말치사량 LPS 전저제량 Dex 간예조。완성실험처치후3 h 취혈표본,응용ELISA방법검측혈청TNF-α화IL-10수평。결과①ⅠA조TNF-α、IL-10수평겁저,ⅠB조TNF-α、IL-10수평교ⅠA조현저증고(P<0．05,P<0．01),Ⅱ조TNF-α、IL-10수평교ⅠB조현저하강(P<0．05,P<0．01),단잉고우ⅠA조。②각Dex간예조TNF-α수평여Ⅱ조비교：ⅢA、ⅣA조TNF-α수평여Ⅱ조TNF-α수평차이무통계학의의(P>0．05),ⅢB、ⅣB조TNF-α수평저우Ⅱ조,차이유통계학의의(P<0．05)。③각Dex간예조IL-10수평여Ⅱ조비교：ⅢA、ⅣA조IL-10수평고우Ⅱ조,차이유통계학의의(P<0．05),ⅢB、ⅣB조IL-10수평여Ⅱ조비교차이무통계학의의(P>0．05)。결론①LPS자격가도치소서체내 TNF-α수평、IL-10수평승고。내독소내수시,소서체내TNF-α、IL-10수평승고적정도명현강저。②종말LPS전일정시간내여이Dex간예가이촉진내독소내수적형성,Dex제량과고가능불회대래경다수익。③IL-10대내독소내수적형성가능불구유결정작용。
Objective To investigate the effects of glucocorticoid on endotoxin tolerance,the formation of en-dotoxin tolerance in mice was intervened by using dexamethasone ( Dex ) . Methods Kunming mice as experimental objects were divided into seven groups. GroupⅠA for healthy control,groupⅠB for once lethal dose lipopolysaccharide (LPS) (2LD50=8 mg/kg) control,groupⅡfor classical endotoxin tolerance,groupⅢA for pretreated high dose Dex (10 mg/kg) before initial LPS stimulation,groupⅢB for pretreated high dose Dex before terminal lethal dose of LPS intervention,groupⅣA for pretreated low dose Dex(1 mg/kg) before initial LPS stimulation,groupⅣB for pretreated low dose Dex before terminal lethal dose of LPS intervention. 3 hours after experimental management,blood specimen was obtained. Enzyme-linked immunosorbent assay was used to detect serum tumour necrosis factor-α(TNF-α),and interleukin-10 (IL-10) levels. Results TNF-α and IL-10 levels of groupⅠA were extremely low,and TNF-αand IL-10 levels of groupⅠB were significantly higher (P<0. 05,P<0. 01). TNF-α and IL-10 levels of groupⅡcompared with that of groupⅠB dropped significantly (P<0. 05,P<0. 01),but which were still higher than that of groupⅠA. The comparison of TNF-α levels of the Dex intervention groups with that of groupⅡ:TNF-α levels of groupⅢA and groupⅣA had no significant difference (P>0. 05). TNF-αlevels of groupⅢB and groupⅣB were lower (P<0. 05). The comparison of IL-10 levels of the Dex intervention groups with that of groupⅡ:IL-10 levels of groupⅢA and groupⅣA were higher (P<0. 05). IL-10 levels of groupⅢB and groupⅣB had no significant differentce (P>0. 05). Conclusion 1. LPS stimulation could elevate TNF-α and IL-10 levels in mice. When mice developed endotoxin toler-ance,their elevated levels of TNF-αand IL-10 decreased obviously. 2. Within a certain duration before terminal LPS in-tervention,pretreatment with Dex could promote the formation of endotoxin tolerance, but too higher Dex might not bring more benefits. 3. IL-10 could not play a decisive role in the formation of endotoxin tolerance.