CAJ | 학술논문

目的探讨雾化吸入布地奈德对博莱霉素致肺纤维化大鼠支气管肺泡灌洗液(BALF)中肿瘤坏死因子α(TNF-α)及血小板衍生生长因子(PDGF)的影响.方法 45只Wistar雌性大鼠随机分为牛理盐水对照组(CG组)、肺纤维化模型组(MG组)、布地奈德干预组(BG组),每组15只.利用博莱霉素建立肺纤维化模型,24 h后给予干预药物,分别于第7天、第14天、第28天处死动物.收集肺组织作切片行HE及Masson染色,观察其病理变化,判断肺组织肺泡炎及肺纤维化程度,测定肺组织羟脯氨酸含量,并测定BALF中TNF-α及PDGF的含量.结果BG组第7天、第14天、第28天肺组织羟脯氦酸含量低于MG组(P<0.05).BG组在早期(第7天、第14天)BALF中TNF-α及PDGF含量低于MG组(P<0.05).结论雾化吸入布地奈德对博莱霉素诱导的肺纤维化大鼠在早期具有较强的抗纤维化效应,机制可能为通过抑制细胞因子TNF-α及PDGF含量的表达,从而有效阻止肺纤维化的进展.
목적 탐토무화흡입포지내덕대박래매소치폐섬유화대서지기관폐포관세액(BALF)중종류배사인자α(TNF-α)급혈소판연생생장인자(PDGF)적영향.방법 45지Wistar자성대서수궤분위우리염수대조조(CG조)、폐섬유화모형조(MG조)、포지내덕간예조(BG조),매조15지.이용박래매소건립폐섬유화모형,24 h후급여간예약물,분별우제7천、제14천、제28천처사동물.수집폐조직작절편행HE급Masson염색,관찰기병리변화,판단폐조직폐포염급폐섬유화정도,측정폐조직간포안산함량,병측정BALF중TNF-α급PDGF적함량.결과BG조제7천、제14천、제28천폐조직간포양산함량저우MG조(P<0.05).BG조재조기(제7천、제14천)BALF중TNF-α급PDGF함량저우MG조(P<0.05).결론 무화흡입포지내덕대박래매소유도적폐섬유화대서재조기구유교강적항섬유화효응,궤제가능위통과억제세포인자TNF-α급PDGF함량적표체,종이유효조지폐섬유화적진전.
Objective To observe the effects of inhaled budesonide on tumor necrosis factor-α(TNF-α) and platelet-derived growth factor (PDGF) in bronchoalveolar lavage fluid (BALF) of bleomycininduced pulmonary fibrosis rats. Methods Forty-five Wistar female rats were randomly divided into control group(CG), pulmonary fibrosis model group(MG) and budesonide intervention group(BG), each group including 15 rats. The model of pulmonary fibrosis was established by a single intratracheal instillation of bleomycin. After 24 hours,both CG and MG were aerosolized 0.9%NaCl solution,while BG was aerosolized budesonide. On the 7th, 14th and 28th day after treatment, five rats of each group were sacrificed,respectively, and their lungs were harvested to examine pathological change, hydroxyproline content in lung tissue. Bronchoalveolar lavage was used to detect the concentration of TNF-α and PDGF in BALF. Results The hydroxyproline concentration in lung tissue of BG was lower than that in MG on the 7th, 14th and 28th day( P <0.05). The levels of TNF-α and PDGF in BALF of BG were lower than those in MG in early stage(7-14 days)( P <0.05). Conclusion Inhaled budesonide, especially in early stage,could ameliorate the formation of bleomycin-induced pulmonary fibrosis through inhibiting the release of TNF-α and PDGF.