中国医药
中國醫藥
중국의약
CHINA MEDICINE
2012年
7期
824-826
,共3页
徐俊马%张衍民%贾晓民%赵杰
徐俊馬%張衍民%賈曉民%趙傑
서준마%장연민%가효민%조걸
肺损伤%氨溴索%Toll样受体4
肺損傷%氨溴索%Toll樣受體4
폐손상%안추색%Toll양수체4
Lung injury%Ambroxol%Toll like receptor 4
目的 探讨氨溴索预处理对大鼠吸人性肺损伤的影响及其作用机制.方法 30只健康SD雄性大鼠按随机数字表法随机分为对照组、损伤组和氨溴索组各10只.对照组大鼠气道内滴人生理盐水,损伤组大鼠气道内滴入胃内容物,氨溴索组大鼠在损伤前给予氨溴索进行干预.观察肺组织湿重/干重比(W/D)、髓过氧化物酶(MPO)活性变化;酶联免疫吸附试验测定血清及肺组织肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)含量;蛋白质印迹法检测肺组织Toll样受体4(TLR4)蛋白表达;光镜下观察肺组织结构变化.结果 损伤组与对照组比较,肺组织湿重/干重比值以及MPO活性增加[(5.01±0.22)比(2.42±0.12)、(3.50±0.24)U/g比(1.10±0.18)U/g,P＜0.05],血清及肺组织中TNF-α、IL1β含量增高[血清:(0.950±0.260) μg/L比(0.075±0.010) μg/L,(0.492±0.046) μg/L比(0.009±0.001)μg/L;肺组织:(0.860±0.160)μg/L比(0.080±0.011 )μg/L、(0.583±0.054)μg/L比(0.007±0.002) μg/L,P＜0.05],TLR4蛋白表达明显增高( 1.98±0.26)比(0.28±0.04)(P＜0.05),肺组织出现明显病理组织学损伤.与损伤组比较,氨溴索组肺组织湿重/干重比值(3.92±0.12)以及MPO活性[(2.76±0.52) U/g]降低(P＜0.05),血清及肺组织中TNF-α[ (0.720±0.130)、(0.620±0.060) μg/L]、IL-1β[ (0.318±0.025)、(0.408±0.036)μg/L]含量降低(P＜0.05),TLR4蛋白表达(1.24±0.15)明显下降(P＜0.05),肺组织病理学损伤减轻.结论 氨溴索预处理对大鼠吸人性肺损伤起防护作用,可能与通过下调TLR4功能抑制促炎症因子表达有关.
目的 探討氨溴索預處理對大鼠吸人性肺損傷的影響及其作用機製.方法 30隻健康SD雄性大鼠按隨機數字錶法隨機分為對照組、損傷組和氨溴索組各10隻.對照組大鼠氣道內滴人生理鹽水,損傷組大鼠氣道內滴入胃內容物,氨溴索組大鼠在損傷前給予氨溴索進行榦預.觀察肺組織濕重/榦重比(W/D)、髓過氧化物酶(MPO)活性變化;酶聯免疫吸附試驗測定血清及肺組織腫瘤壞死因子α(TNF-α)、白細胞介素1β(IL-1β)含量;蛋白質印跡法檢測肺組織Toll樣受體4(TLR4)蛋白錶達;光鏡下觀察肺組織結構變化.結果 損傷組與對照組比較,肺組織濕重/榦重比值以及MPO活性增加[(5.01±0.22)比(2.42±0.12)、(3.50±0.24)U/g比(1.10±0.18)U/g,P＜0.05],血清及肺組織中TNF-α、IL1β含量增高[血清:(0.950±0.260) μg/L比(0.075±0.010) μg/L,(0.492±0.046) μg/L比(0.009±0.001)μg/L;肺組織:(0.860±0.160)μg/L比(0.080±0.011 )μg/L、(0.583±0.054)μg/L比(0.007±0.002) μg/L,P＜0.05],TLR4蛋白錶達明顯增高( 1.98±0.26)比(0.28±0.04)(P＜0.05),肺組織齣現明顯病理組織學損傷.與損傷組比較,氨溴索組肺組織濕重/榦重比值(3.92±0.12)以及MPO活性[(2.76±0.52) U/g]降低(P＜0.05),血清及肺組織中TNF-α[ (0.720±0.130)、(0.620±0.060) μg/L]、IL-1β[ (0.318±0.025)、(0.408±0.036)μg/L]含量降低(P＜0.05),TLR4蛋白錶達(1.24±0.15)明顯下降(P＜0.05),肺組織病理學損傷減輕.結論 氨溴索預處理對大鼠吸人性肺損傷起防護作用,可能與通過下調TLR4功能抑製促炎癥因子錶達有關.
목적 탐토안추색예처리대대서흡인성폐손상적영향급기작용궤제.방법 30지건강SD웅성대서안수궤수자표법수궤분위대조조、손상조화안추색조각10지.대조조대서기도내적인생리염수,손상조대서기도내적입위내용물,안추색조대서재손상전급여안추색진행간예.관찰폐조직습중/간중비(W/D)、수과양화물매(MPO)활성변화;매련면역흡부시험측정혈청급폐조직종류배사인자α(TNF-α)、백세포개소1β(IL-1β)함량;단백질인적법검측폐조직Toll양수체4(TLR4)단백표체;광경하관찰폐조직결구변화.결과 손상조여대조조비교,폐조직습중/간중비치이급MPO활성증가[(5.01±0.22)비(2.42±0.12)、(3.50±0.24)U/g비(1.10±0.18)U/g,P＜0.05],혈청급폐조직중TNF-α、IL1β함량증고[혈청:(0.950±0.260) μg/L비(0.075±0.010) μg/L,(0.492±0.046) μg/L비(0.009±0.001)μg/L;폐조직:(0.860±0.160)μg/L비(0.080±0.011 )μg/L、(0.583±0.054)μg/L비(0.007±0.002) μg/L,P＜0.05],TLR4단백표체명현증고( 1.98±0.26)비(0.28±0.04)(P＜0.05),폐조직출현명현병리조직학손상.여손상조비교,안추색조폐조직습중/간중비치(3.92±0.12)이급MPO활성[(2.76±0.52) U/g]강저(P＜0.05),혈청급폐조직중TNF-α[ (0.720±0.130)、(0.620±0.060) μg/L]、IL-1β[ (0.318±0.025)、(0.408±0.036)μg/L]함량강저(P＜0.05),TLR4단백표체(1.24±0.15)명현하강(P＜0.05),폐조직병이학손상감경.결론 안추색예처리대대서흡인성폐손상기방호작용,가능여통과하조TLR4공능억제촉염증인자표체유관.
Objective To investigate the effects and mechanisms of ambroxol pretreatment on rats' gastric aspiration lung injury.Metbods Thirty Sprague-Dawley rats were randomly divided into three equal groups:eontrolgroup,injury group and ambroxol group.In the control group,physiologic saline was instilled into the trachea of the rats;in the injury group,gastric content was instilled into the trachea of the rats;in the ambroxol group,ambroxol was injected before the injury was carried out.Wet-to-dry weight ratio(W/D) of lung and the activity of myeloperoxidase(MPO) were measured;tumor necrosis factor-or(TNF-α) and interlcukin-lβ(IL-Iβ) of scrum and lung homogenate were examined by enzyme linked immunosorbent assay(ELISA).Toll like receptor 4(TLR4) was examined by Western blot.Lung pathological change was observed by microscope.Results Compared with control group,W/D of lung,the activity of MPO,TNF-α and IL-1β3 of serum/lung homogenate,TLR4 expression in Injury group increased[(5.01±0.22)vs(2.42±0.12),(3.50±0.24) U/g vs(1.10±0.18) U/g,serum:(0.950±0.260) μg/L vs(0.075±0.010) μg/L,(0.492±0.046) μg/L vs(0.009±0.001)μg/L;lung:(0.860±0.160)μg/L vs(0.080±0.011)μg/L,(0.583±0.054)μg/L vs(0.007±0.002)μg/L,p ＜0.05].Compared with injury group,W/D of lung(3.92±0.12),the activity of MPO [(2.76±0.52) U/g ],TNF-α and IL-1 β of serum/lung homogenate and TLR4 expression(1.24±0.15) in ambroxol group decreased(P ＜ 0.05).The microscopic structure of the control group was normal and the pathological changes of ambroxol group were milder than those of injury group.Conclusions Ambroxol pretreatment shows protective effects on gastric aspiration lung injury.The mechanism may relate to down-regulation of TLR4 and inhibit the expression of pro-inflammatory cytokins.
