CAJ | 학술논문

目的：：探讨脂多糖(LPS)对哮喘小鼠肥大细胞活化及p38蛋白激酶(p38MAPK)表达的影响。方法：将24只BALB/c小鼠随机分为3组：A(哮喘组)、B(0.1mg LPS+OVA组)、C(对照组),每组8只,采用免疫佐剂(氢氧化铝)与卵清蛋白(OVA)腹腔注射致敏及用1%OVA生理盐水雾化激发的方法制备哮喘小鼠模型。采用免疫组织化学染色SP法半定量测定肺组织中类胰蛋白酶及p38MAPK表达的情况,HE染色观察肺组织病理变化。结果：与A组相比,B组小鼠肺组织类胰蛋白酶及p38MAPK的MOD显著升高(P<0.05)；光镜下,A组支气管黏膜下水肿,管壁平滑肌肥大,基底膜增厚,黏膜皱襞增多,气道、血管周围间质可见大量嗜酸性粒细胞、中性粒细胞、淋巴细胞为主的炎症细胞浸润。B组上述情况未减轻,并出现肺泡腔及间质充血。C组气道周围无炎症细胞浸润,肺泡壁结构完整。结论：LPS可明显加重哮喘气道炎症,表明部分机制可能是通过影响肥大细胞活化及p38MAPK信号通路实现的。
목적：：탐토지다당(LPS)대효천소서비대세포활화급p38단백격매(p38MAPK)표체적영향。방법：장24지BALB/c소서수궤분위3조：A(효천조)、B(0.1mg LPS+OVA조)、C(대조조),매조8지,채용면역좌제(경양화려)여란청단백(OVA)복강주사치민급용1%OVA생리염수무화격발적방법제비효천소서모형。채용면역조직화학염색SP법반정량측정폐조직중류이단백매급p38MAPK표체적정황,HE염색관찰폐조직병리변화。결과：여A조상비,B조소서폐조직류이단백매급p38MAPK적MOD현저승고(P<0.05)；광경하,A조지기관점막하수종,관벽평활기비대,기저막증후,점막추벽증다,기도、혈관주위간질가견대량기산성립세포、중성립세포、림파세포위주적염증세포침윤。B조상술정황미감경,병출현폐포강급간질충혈。C조기도주위무염증세포침윤,폐포벽결구완정。결론：LPS가명현가중효천기도염증,표명부분궤제가능시통과영향비대세포활화급p38MAPK신호통로실현적。
Objective:To investigate the effects of lipopolysaccharide on activation of mast cell and the expression of p38 mitogen-activated protein kinase (p38MAPK) in asthmatic mice.Methods:Twenty-four BALB/c mice were randomly assigned to three groups,group A(asthma group)、group B(0.1mg LPS+OVA group)、group C(control group), with 8 mice in each group. Mice in the group A and group B were treated with adiuvant (aluminum hydroxide) and chicken ovallbumin (OVA).The expression of tryptase and p38MAPK were semi-quantitative detection by using immunohistochemistry sp method and the pathologic changes of lung tissue were observed by HE stain.Results:The results of immunohistochemical determination showed that lung tissue of mice tryptase and p38MAPK in the group B more than those of the group A(P<0.05).The lung tissue from group A showed bronchial submucosal edema,smooth muscle hypertrophy,basementmembra thickening,mucosa plica increasing,inflammatory cells infiltration in the peribronchovascular interstitium.Bisides,the lung tissue of group B was also obviously observed alveolar and infiltration hyperemia.So the pathological changes in the group B were worse than that of the group A.However,the group C was no inflammation cell around airway.Conclusion:The results of LPS exacerbating airway inflammation in asthma may be achieved by influencing by the activation of mast cells and influencing p38MAPK signal pathway.