国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2008年
20期
1221-1223,封3
,共4页
杨敬平%李姝楠%孙德俊%高丽
楊敬平%李姝楠%孫德俊%高麗
양경평%리주남%손덕준%고려
肺间质纤维化%肌纤维母细胞%α平滑肌肌动蛋白%Ⅰ型胶原
肺間質纖維化%肌纖維母細胞%α平滑肌肌動蛋白%Ⅰ型膠原
폐간질섬유화%기섬유모세포%α평활기기동단백%Ⅰ형효원
Pulmonary interstitial fibrosis%Myofibroblast%α-smooth muscle actin%Ⅰ-collagen
目的 探讨α平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)在肺间质纤维化中的意义.方法 发将64只Wistar大鼠随机分为对照组和博莱霉素模型组.在第3天、第7天、第14天和第28天,HE染色观察大鼠肺组织结构的改变,免疫组织化学法测定肺组织α-SMA和Ⅰ型胶原的表达,同时用流式细胞术检测肺组织单细胞悬液α-SMA的相对含量.结果 博莱霉素模型组大鼠肺组织α-SMA和Ⅰ型胶原的表达在各时间段均高于对照组(P<0.05),并且两种因子表达呈正相关.同时,博莱霉素模型组各时间段两种因子测定结果 均结果 的差异有统计学意义(P<0.05).结论 经 肺间质纤维化大鼠肺组织α-SMA表达增高,预示肌纤维母细胞的形成,导致Ⅰ型胶原堆积,从而引起肺纤维化.
目的 探討α平滑肌肌動蛋白(α-smooth muscle actin,α-SMA)在肺間質纖維化中的意義.方法 髮將64隻Wistar大鼠隨機分為對照組和博萊黴素模型組.在第3天、第7天、第14天和第28天,HE染色觀察大鼠肺組織結構的改變,免疫組織化學法測定肺組織α-SMA和Ⅰ型膠原的錶達,同時用流式細胞術檢測肺組織單細胞懸液α-SMA的相對含量.結果 博萊黴素模型組大鼠肺組織α-SMA和Ⅰ型膠原的錶達在各時間段均高于對照組(P<0.05),併且兩種因子錶達呈正相關.同時,博萊黴素模型組各時間段兩種因子測定結果 均結果 的差異有統計學意義(P<0.05).結論 經 肺間質纖維化大鼠肺組織α-SMA錶達增高,預示肌纖維母細胞的形成,導緻Ⅰ型膠原堆積,從而引起肺纖維化.
목적 탐토α평활기기동단백(α-smooth muscle actin,α-SMA)재폐간질섬유화중적의의.방법 발장64지Wistar대서수궤분위대조조화박래매소모형조.재제3천、제7천、제14천화제28천,HE염색관찰대서폐조직결구적개변,면역조직화학법측정폐조직α-SMA화Ⅰ형효원적표체,동시용류식세포술검측폐조직단세포현액α-SMA적상대함량.결과 박래매소모형조대서폐조직α-SMA화Ⅰ형효원적표체재각시간단균고우대조조(P<0.05),병차량충인자표체정정상관.동시,박래매소모형조각시간단량충인자측정결과 균결과 적차이유통계학의의(P<0.05).결론 경 폐간질섬유화대서폐조직α-SMA표체증고,예시기섬유모세포적형성,도치Ⅰ형효원퇴적,종이인기폐섬유화.
Objective To investigate the expression of α-smooth muscle actin (α-SMA) andⅠ-collagen(col-Ⅰ) in pathogenesis of pulmonary interstitial fibrosis. Methods Sixty-four Wistar rats weredivided into two groups, control group: instilled normal saline into trachea and bleomycin (BM) group:instilled BM into trachea. The course was sacrificed 3,7,14,28 days and at each time-point, the lung tissuemorphological changes were examined by histopathology, α-SMA and col-Ⅰ expressions were studied byimmunohistochemistry. Flow cytometry was utilized to quantitatively detect the precision of α-SMA in a cellsuspension of lung tissues. Results At all time-points, lung tissues α-SMA and col-Ⅰ increasedsignificantly in BM group than that in control group ( P < 0.05). Expression of col-Ⅰ was positivelycorrelated with that of α-SMA. There was significant differenee between expression of α-SMA and that ofcol-Ⅰ in BM group at all time-points( P<0.05). Conculusions The increase of α-SMA in pulmonary tissuesof BM-induced pulmonary fibrosis rats suggests the formation of myofibroblast, which may be involved inaccumulation of col-Ⅰ and contributed to pulmonary fibrosis.