CAJ | 학술논문

目的：探讨波生坦对肺间质纤维化（PIF）大鼠肺血管病变的影响。方法将24只成年雄性Wistar大鼠随机均分为3组：对照组（C组）、模型组（F组）和治疗组（T组），n=8；予博来霉素建立PIF模型；T组于第2天始予波生坦（100mg/kg.d）灌胃治疗,C、F组予等量生理盐水对照。4周末测定各组大鼠血浆内皮素-1（ET-1）水平，光镜下观察肺血管病理改变。结果1.C组、F组、T组血浆ET-1分别为0.11±0.04、0.41±0.13、0.27±0.04（ng/m1）；2.F组比较于C组明显升高，（P＜0.05），波生坦治疗的T组较F组下降，差异有显著性意义。3.肺血管病理：C组大鼠血管内皮完整，基底膜线状连续；模型F组血管外肺泡充填大量炎性细胞，多处血管内皮细胞坏死，内膜结构不清甚至断裂，管壁明显增厚，部分闭塞；治疗T组较F组肺血管内皮相对完整，血管平滑肌增殖及管腔狭窄明显减轻。结论波生坦可以通过拮抗并降低ET-1水平，减少肺血管损伤，延缓肺间质纤维化的进展。
목적：탐토파생탄대폐간질섬유화（PIF）대서폐혈관병변적영향。방법장24지성년웅성Wistar대서수궤균분위3조：대조조（C조）、모형조（F조）화치료조（T조），n=8；여박래매소건립PIF모형；T조우제2천시여파생탄（100mg/kg.d）관위치료,C、F조여등량생리염수대조。4주말측정각조대서혈장내피소-1（ET-1）수평，광경하관찰폐혈관병리개변。결과1.C조、F조、T조혈장ET-1분별위0.11±0.04、0.41±0.13、0.27±0.04（ng/m1）；2.F조비교우C조명현승고，（P＜0.05），파생탄치료적T조교F조하강，차이유현저성의의。3.폐혈관병리：C조대서혈관내피완정，기저막선상련속；모형F조혈관외폐포충전대량염성세포，다처혈관내피세포배사，내막결구불청심지단렬，관벽명현증후，부분폐새；치료T조교F조폐혈관내피상대완정，혈관평활기증식급관강협착명현감경。결론파생탄가이통과길항병강저ET-1수평，감소폐혈관손상，연완폐간질섬유화적진전。
Objective To investigate the effects of bosentan on pulmonary vascular lesions of bleomycin-induced pulmonary interstitial fibrosis (PIF) in rats . Methods 24 male adult Wistar rats were randomly divided into control groups(C group),model groups(F group) and treated groups(T group). The plasma ET-1 was measured after 4 weeks and pulmonary vascular pathology was observed. Results 1.The levels of plasma ET-1 in the C.F and T group were 0.11±0.04、0.41±0.13 and 0.27±0.04 (ng/m1) respectively. 2. The level of ET-1 in F group was higher than C group, and T group decreased significantly compared to F group. 3. The vascular endothelium in C group was complete. Multiple vascula endothelial destruction was found in F group and the vascula wal was thickening even occlusive. Pulmonary vascular endothelial integrity, vascular proliferation and tube smooth muscle constriction significantly improved in T group. Conclusion Bosentan can protect against the pulmonary vascular lesions of PIF induced by bleomycin and delay the disease progression of PIF through reducing and blocking the ET-1.