CAJ | 학술논문

目的：探讨木犀草素抑制哮喘大鼠气道炎症的可能机制.方法取健康清洁级Wistar大鼠60只,随机分为木犀草素组、哮喘组、对照组,每组各20只.木犀草素组、哮喘组建立大鼠哮喘模型,建模过程中每次激发后1 h给予哮喘组和对照组腹腔注射生理盐水,木犀草素组腹腔注射1 mg/kg的木犀草素.光镜下观察大鼠肺组织病理变化,测定支气管肺泡灌洗液中的细胞数及IL-4水平；免疫组化法检测p38MAPK,PPARγ蛋白表达情况；RT-PCR检测p38MAPK,PPARγ的相对表达量.结果3组大鼠支气管基底膜周径之间差异无统计学意义( P>0.05)；哮喘组大鼠平滑肌厚度、管壁厚度均明显高于对照组及木犀草素组大鼠(P<0.05).哮喘组大鼠细胞总数、嗜酸粒细胞数、中性粒细胞数均明显高于木犀草素组和对照组(P<0.05)；木犀草素组细胞总数、嗜酸粒细胞数、中性粒细胞数均明显高于对照组(P<0.05)；哮喘组IL-4含量明显高于木犀草素组及对照组(P<0.05)；哮喘组大鼠p38MAPK蛋白表达明显高于对照组,PPARγ蛋白表达明显低于对照组(P<0.05)；木犀草素组大鼠p38MAPK蛋白表达明显低于哮喘组,PPARγ蛋白表达明显高于哮喘组(P<0.05).哮喘组大鼠p38MAPK mRNA相对表达量明显高于对照组,木犀草素组表达量明显低于哮喘组(P<0.05)；哮喘组大鼠PPARγ mRNA相对表达量明显低于对照组,木犀草素组表达量明显高于哮喘组(P<0.05).结论木犀草素可能通过影响PPARγ表达和p38MAPK信号通路而发挥抑制哮喘大鼠气道炎症的作用.
목적：탐토목서초소억제효천대서기도염증적가능궤제.방법취건강청길급Wistar대서60지,수궤분위목서초소조、효천조、대조조,매조각20지.목서초소조、효천조건립대서효천모형,건모과정중매차격발후1 h급여효천조화대조조복강주사생리염수,목서초소조복강주사1 mg/kg적목서초소.광경하관찰대서폐조직병리변화,측정지기관폐포관세액중적세포수급IL-4수평；면역조화법검측p38MAPK,PPARγ단백표체정황；RT-PCR검측p38MAPK,PPARγ적상대표체량.결과3조대서지기관기저막주경지간차이무통계학의의( P>0.05)；효천조대서평활기후도、관벽후도균명현고우대조조급목서초소조대서(P<0.05).효천조대서세포총수、기산립세포수、중성립세포수균명현고우목서초소조화대조조(P<0.05)；목서초소조세포총수、기산립세포수、중성립세포수균명현고우대조조(P<0.05)；효천조IL-4함량명현고우목서초소조급대조조(P<0.05)；효천조대서p38MAPK단백표체명현고우대조조,PPARγ단백표체명현저우대조조(P<0.05)；목서초소조대서p38MAPK단백표체명현저우효천조,PPARγ단백표체명현고우효천조(P<0.05).효천조대서p38MAPK mRNA상대표체량명현고우대조조,목서초소조표체량명현저우효천조(P<0.05)；효천조대서PPARγ mRNA상대표체량명현저우대조조,목서초소조표체량명현고우효천조(P<0.05).결론목서초소가능통과영향PPARγ표체화p38MAPK신호통로이발휘억제효천대서기도염증적작용.
Objective To explore the possible inhibition mechanism of luteolin on airway inflammation in asthmatic rats. Method Sixty healthy Wistar rats were randomly divided into 3 groups, luteolin group, asthma group and control group, with 20 rats in each group. At the 1st hour after each excitation in the process of modeling,the asthma group and control group accepted intraperitoneal injection of saline,and the luteolin group was administrated with 1 mg/kg of luteolin. The pathological changes of lung tissue were observed under light microscope,and the cell number and IL-4 level in bronchoalveolar lavage fluid were measured. The expressions of PPARγ and p38MAPK were detected by immunohistochemistry,and the relative expressions of p38MAPK and PPARγ were detected by RT-PCR. Results The bronchial basement membrane perimeter of the rats in three groups showed no significant difference ( P>0 . 05 );but the thicknesses of smooth muscle and tube wall of the asthmatic rats were significantly higher than those in the control group and luteolin treated rats ( P<0 . 05 ) . The number of total cells,eosinophil cell and neutral granular cell of the rats in asthma group were significantly higher than those of the luteolin group and the control group ( P<0 . 05 ) , the cells number of luteolin group was significantly higher than those of the control group (P <0. 05),and the content of IL-4 in asthma group was significantly higher than that of luteolin group and control group (P<0. 05). Compared with the control group,the expressions of p38MAPK and PPARγ in asthma rats were significantly higher(P <0. 05). The expression of p38MAPK in luteolin group was much lower than the asthma group,and the expression of PPARγ is higher (P<0. 05). The relative expression of p38MAPK mRNA in asthmatic group was significantly higher than that of the control group,and the expression in luteolin group was significantly lower than that in the asthma group (P<0. 05). The relative expression of PPAR mRNA in asthma group was significantly lower than that of the control group, and the expression in luteolin group was significantly higher than that in the asthma group (P<0. 05). Conclusion Luteolin may inhibit the airway inflammation in asthmatic rats by influencing the expression of PPARγ and the signal pathway of p38MAPK.