CAJ | 학술논문

目的：探讨内源性硫化氢(H 2 S)对于吸烟诱导的 COPD 大鼠模型中小气道纤维化的影响。方法32只健康雄性 SD 大鼠随机分为正常组、吸烟组、吸烟+H 2 S 组和吸烟+炔丙基甘氨酸(PPG)组,采用被动烟雾吸入法,共吸烟4个月,从第3个月起,每日吸烟前给予大鼠腹腔注射生理盐水、硫氢化钠(NaHS)(14μmol/kg)或 PPG(37.5 mg/kg),取肺组织切片进行 HE 染色和天狼星红染色,观察肺组织病理形态改变,对小气道胶原沉积采用半定量分析,并进行小气道病理评分。Western blot 检测肺组织胱硫醚-γ-裂解酶(CGL)、Ⅰ型胶原蛋白表达水平。结果与正常组比较,吸烟组小气道病理评分明显升高(P <0.01),NaHS 干预后较吸烟组评分降低(P <0.05)。偏振光显微镜下观察天狼星红染色切片,吸烟组和吸烟+PPG 组较正常组小气道周围胶原沉积显著增多(P <0.01),吸烟+ H 2 S 组较吸烟组明显减少(P <0.05)。与正常组相比,吸烟组大鼠肺组织Ⅰ型胶原蛋白含量明显增多(P <0.05),NaHS干预后Ⅰ型胶原蛋白含量较单纯吸烟组明显降低(P <0.05)。结论内源性 H 2 S 参与吸烟诱导的COPD 大鼠小气道纤维化的病理生理过程,外源性给予 H 2 S 对小气道纤维化具有保护作用。
목적：탐토내원성류화경(H 2 S)대우흡연유도적 COPD 대서모형중소기도섬유화적영향。방법32지건강웅성 SD 대서수궤분위정상조、흡연조、흡연+H 2 S 조화흡연+결병기감안산(PPG)조,채용피동연무흡입법,공흡연4개월,종제3개월기,매일흡연전급여대서복강주사생리염수、류경화납(NaHS)(14μmol/kg)혹 PPG(37.5 mg/kg),취폐조직절편진행 HE 염색화천랑성홍염색,관찰폐조직병리형태개변,대소기도효원침적채용반정량분석,병진행소기도병리평분。Western blot 검측폐조직광류미-γ-렬해매(CGL)、Ⅰ형효원단백표체수평。결과여정상조비교,흡연조소기도병리평분명현승고(P <0.01),NaHS 간예후교흡연조평분강저(P <0.05)。편진광현미경하관찰천랑성홍염색절편,흡연조화흡연+PPG 조교정상조소기도주위효원침적현저증다(P <0.01),흡연+ H 2 S 조교흡연조명현감소(P <0.05)。여정상조상비,흡연조대서폐조직Ⅰ형효원단백함량명현증다(P <0.05),NaHS간예후Ⅰ형효원단백함량교단순흡연조명현강저(P <0.05)。결론내원성 H 2 S 삼여흡연유도적COPD 대서소기도섬유화적병리생리과정,외원성급여 H 2 S 대소기도섬유화구유보호작용。
Objective To investigate the effect of hydrogen sulfide (H 2 S)in small airway fibrosis of rats with chronic obstructive pulmonary disease (COPD).Methods Thirty-two male Sprague-Dawley rats were randomly divided into four groups:control group,tobacco smoke group,smoke+H 2 S group,and smoke+PPG group.Drug intervention started at the third month of a total four-month smoke exposure. Rats were intraperitoneally injected with normal saline,sodium hydrosulfide (NaHS,14 μmol/kg),or PPG (37.5 mg/kg)before smoke every day.After four months,the histological change of lungs and the collagen deposition in airway were measured by HE staining and picrosiriu-red staining.The pathological score of small airway was calculated.The expressions of cystathionine γ-lyase and collagen Ⅰ were measured by Western blot.Results Compared with control group,the pathological score of small airway was significantly elevated in smoke group (P < 0.01 ),but decreased after NaHS intervention (P <0.05).Picrosiriu-red staining was detected under a polarided microscope.Compared with control group, the collagen deposition around the airway wall was increased in smoke group and smoke+PPG group (P <0.01).And the collagen deposition in smoke+H 2 S group was less than that in smoke group (P <0.05). Compared with control group,the expression of collagenⅠwas significant elevated in smoke group (P <0.05),but decreased after NaHS intervention (P <0.05).Conclusions Endogenous H 2 S plays a crucial role in the small airway fibrosis in smoke-induced COPD rats.Exogenously applied H 2 S could attenuate the process of airway fibrosis.