国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2010年
3期
218-221
,共4页
利多卡因%哮喘%热休克蛋白70%核因子κB
利多卡因%哮喘%熱休剋蛋白70%覈因子κB
리다잡인%효천%열휴극단백70%핵인자κB
Lidocaine%Asthma%Heat shock protein 70%Nuclear factor-kappe B
目的 观察利多卡因对大鼠支气管哮喘模型肺组织中热休克蛋白70(heat shock protein 70,HSP70)、核因子κB(nuclear factor-kappe B,NF-κB)表达的影响.方法 Wistar大鼠32只,随机分为4组(n=8):对照组(A组)、哮喘组(B组)、地塞米松组(C组)、利多卡因组(D组).B组大鼠用鸡卵清蛋白辅以氢氧化铝为佐剂注射致敏,2周后雾化吸入鸡卵清蛋白诱发哮喘;C组、D组大鼠用同样方法致敏,但在激发前分别雾化吸入0.02%地寒米松和0.04%利多卡因20 ml;A组用生理盐水代替鸡卵清蛋白进行注射和吸入.末次雾化吸人后24 h内取肺组织,计算湿十重比(W/D)、观察肺组织病理学改变、免疫组化检测HSP70、NF-κB的表达.结果 ①B、C、D组W/D值分别为4.08±0.16、3.54±0.10和3.66±0.12,和A组3.30±0.12相比增加(P<0.05);②B、C、D组肺组织HSP70表达分别为0.210±0.018、0.138±0.010和0.154±0.012,和A组0.049±0.015相比表达上调(P<0.05);③B、C、D组肺组织NF-κB表达分别为0.199±0.029、0.132±0.010和0.150±0.017,和A组0.056±0.022相比表达上调(P<0.05);④和B组相比,C、D组W/D值、肺组织HSP70、NF-κB的表达下调(P<0.05).B组肺组织呈支气管壁增厚、炎性细胞浸润表现.C组、D组病理损伤程度减轻. 结论利多卡因雾化吸入可以减轻致敏原所激发的哮喘大鼠气道炎症和肺组织损伤.
目的 觀察利多卡因對大鼠支氣管哮喘模型肺組織中熱休剋蛋白70(heat shock protein 70,HSP70)、覈因子κB(nuclear factor-kappe B,NF-κB)錶達的影響.方法 Wistar大鼠32隻,隨機分為4組(n=8):對照組(A組)、哮喘組(B組)、地塞米鬆組(C組)、利多卡因組(D組).B組大鼠用鷄卵清蛋白輔以氫氧化鋁為佐劑註射緻敏,2週後霧化吸入鷄卵清蛋白誘髮哮喘;C組、D組大鼠用同樣方法緻敏,但在激髮前分彆霧化吸入0.02%地寒米鬆和0.04%利多卡因20 ml;A組用生理鹽水代替鷄卵清蛋白進行註射和吸入.末次霧化吸人後24 h內取肺組織,計算濕十重比(W/D)、觀察肺組織病理學改變、免疫組化檢測HSP70、NF-κB的錶達.結果 ①B、C、D組W/D值分彆為4.08±0.16、3.54±0.10和3.66±0.12,和A組3.30±0.12相比增加(P<0.05);②B、C、D組肺組織HSP70錶達分彆為0.210±0.018、0.138±0.010和0.154±0.012,和A組0.049±0.015相比錶達上調(P<0.05);③B、C、D組肺組織NF-κB錶達分彆為0.199±0.029、0.132±0.010和0.150±0.017,和A組0.056±0.022相比錶達上調(P<0.05);④和B組相比,C、D組W/D值、肺組織HSP70、NF-κB的錶達下調(P<0.05).B組肺組織呈支氣管壁增厚、炎性細胞浸潤錶現.C組、D組病理損傷程度減輕. 結論利多卡因霧化吸入可以減輕緻敏原所激髮的哮喘大鼠氣道炎癥和肺組織損傷.
목적 관찰리다잡인대대서지기관효천모형폐조직중열휴극단백70(heat shock protein 70,HSP70)、핵인자κB(nuclear factor-kappe B,NF-κB)표체적영향.방법 Wistar대서32지,수궤분위4조(n=8):대조조(A조)、효천조(B조)、지새미송조(C조)、리다잡인조(D조).B조대서용계란청단백보이경양화려위좌제주사치민,2주후무화흡입계란청단백유발효천;C조、D조대서용동양방법치민,단재격발전분별무화흡입0.02%지한미송화0.04%리다잡인20 ml;A조용생리염수대체계란청단백진행주사화흡입.말차무화흡인후24 h내취폐조직,계산습십중비(W/D)、관찰폐조직병이학개변、면역조화검측HSP70、NF-κB적표체.결과 ①B、C、D조W/D치분별위4.08±0.16、3.54±0.10화3.66±0.12,화A조3.30±0.12상비증가(P<0.05);②B、C、D조폐조직HSP70표체분별위0.210±0.018、0.138±0.010화0.154±0.012,화A조0.049±0.015상비표체상조(P<0.05);③B、C、D조폐조직NF-κB표체분별위0.199±0.029、0.132±0.010화0.150±0.017,화A조0.056±0.022상비표체상조(P<0.05);④화B조상비,C、D조W/D치、폐조직HSP70、NF-κB적표체하조(P<0.05).B조폐조직정지기관벽증후、염성세포침윤표현.C조、D조병리손상정도감경. 결론리다잡인무화흡입가이감경치민원소격발적효천대서기도염증화폐조직손상.
Objective To observe the effect of aerosolized lidocaine inhalation on expression of HSP70 and NF-ΚB in lung of asthma rat model. Methods Thirty two Wistar rats were randomly assigned to four groups (n=8 each): control group( group A), asthma model group(group B),dexamethasone group(group C)and lidocaine group(group D). The rats in group B were sensitized by injection of ovalbumin(OA )together with aluminum hydroxide as adjuvants, followed by aerosolized OA challenge two weeks later. The rats in group C and D were sensitized with OA as group B, but exposed to 0.02% aerosol of dexamethasone and 0.04% aerosol of lidocaine 20 ml respectively. In group A saline was used instead of OA. In 24 hours after the last challenge, the lungs were removed for microscopic examination, determination of W/D lung weight radio, the expression of HSP70 and NF-ΚB was studied immunohistochemically.Results①The W/D lung weight radio were 4.08±0.16,3.54±0.10 and 3.66±0.12 respectively in group B,C,D,more than the group A with 3.30±0.12. ② The pulmonary expression of HSP70 were 0.210±0.018,0.138±0.010 and 0.154±0.012 respectively in group B,C,D, higher than the group A with 0.049±0.015. ③The pulmonary expression of NF -KB were 0.199±0.029,0.132±0.010 and 0.150±0.017respectively in group B, C, D, higher than the group A with 0.056±0.022. ④Compared with the group B, the W/D lung weight radio and pulmonary expression of HSP70 and NF -ΚB in group C and D were significantly down -regulated. In animals with asthma the bronchial walls were significantly thicker with inflammatory cell infiltration. Dexamethasone or lidocaine aerosolized inhalation significantly attenuated the pathologic changes induced by asthma. Conclusion Aerosolized lidocaine inhalation has a protective effect on airway inflammation and histology damages resulting from aeroallergen challenge in the asthma model of Wistar rats.
