CAJ | 학술논문

目的探讨盐酸氨溴索对慢性阻塞性肺疾病急性加重（AECOPD）患者p38丝裂原活化蛋白激酶（p38MAPK）通路的影响。方法90例AECOPD患者在给予抗感染、解痉平喘等对症支持治疗的基础上，根据应用祛痰药物不同，随机分为生理盐水组、溴己新组、氨溴索组，每组30例，监测治疗过程中白细胞计数（WBC ）、中性粒细胞比例（N％）、超敏C-反应蛋白（hs-CRP）、红细胞沉降率（ESR）变化；测定3组患者入院当天及用药治疗7 d后血清中p38MAPK、白细胞介素（IL）-8、IL-10的变化情况。结果经治疗后患者血常规、CRP、ESR较治疗前明显下降；并且氨溴索组改善情况优于溴己新组；氨溴索组治疗后第7天，与生理盐水组、溴已新组治疗后第7天比较，以氨溴索组的p38M A PK、IL-8、IL-10下降最明显，3组比较差异有统计学意义（ P＜0．01）。结论氨溴索通过下调p38MAPK通路活化，调节AECOPD患者血清IL-8、IL-10，是其抗炎作用机制之一。
목적탐토염산안추색대만성조새성폐질병급성가중（AECOPD）환자p38사렬원활화단백격매（p38MAPK）통로적영향。방법90례AECOPD환자재급여항감염、해경평천등대증지지치료적기출상，근거응용거담약물불동，수궤분위생리염수조、추기신조、안추색조，매조30례，감측치료과정중백세포계수（WBC ）、중성립세포비례（N％）、초민C-반응단백（hs-CRP）、홍세포침강솔（ESR）변화；측정3조환자입원당천급용약치료7 d후혈청중p38MAPK、백세포개소（IL）-8、IL-10적변화정황。결과경치료후환자혈상규、CRP、ESR교치료전명현하강；병차안추색조개선정황우우추기신조；안추색조치료후제7천，여생리염수조、추이신조치료후제7천비교，이안추색조적p38M A PK、IL-8、IL-10하강최명현，3조비교차이유통계학의의（ P＜0．01）。결론안추색통과하조p38MAPK통로활화，조절AECOPD환자혈청IL-8、IL-10，시기항염작용궤제지일。
Objective To investigate the effect of hydrochloride ambroxol on p38 MAP kinase pathway in pa-tients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) .Methods 90 patients with AE-COPD were divided into different groups according to expectorant drugs prescribed after anti-infection ,spasmolysis and other supportive treatment ,including saline group ,bromhexine group and ambroxol group ,30 cases for each group .White blood cell counting (WBC) ,neutrophil ratio (N% ) ,high sensitive C reactive protein (hs-CRP) and e-rythrocyte sedimentation rate (ESR) were monitored during treatment .Serum levels of p38MAPK ,interleukin (IL)-8 and IL-10 were detected at the 1st and 7th day of treatment .Results After treatment ,WBC ,CRP and ESR levels significantly decreased ,and ambroxol group might be better than bromhexine group .At the 7th day of treatment , the deceasing tendency of p38MAPK ,IL-8 and IL-10 in ambroxol group was more significant than saline group and bromhexine group ,and there were significant differences between the three groups (P<0 .01) .Conclusion Ambr-oxol could regulate serum levels of IL-8 and IL-10 by down-regulation of p38MAPK pathway activation in patients with AECOPD ,which might be its anti-inflammatory mechanism in AECOPD .