中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2011年
2期
103-107
,共5页
胡迎春%罗振华%袁新健%杨丽萍%王守凤%李广悦%贺性鹏
鬍迎春%囉振華%袁新健%楊麗萍%王守鳳%李廣悅%賀性鵬
호영춘%라진화%원신건%양려평%왕수봉%리엄열%하성붕
铀矿尘%肺纤维化%Ⅰ型胶原、Ⅲ型胶原%层粘连蛋白
鈾礦塵%肺纖維化%Ⅰ型膠原、Ⅲ型膠原%層粘連蛋白
유광진%폐섬유화%Ⅰ형효원、Ⅲ형효원%층점련단백
Uranium ore dust%Lung fibrosis%ⅠCollagen%Ⅲ Collagen%LN
目的 探讨铀矿尘致大鼠纤维化过程中Ⅰ、Ⅲ型胶原、层粘连蛋白(Laminin,LN)表达的变化特征.方法 60只Wistar大鼠随机分为铀矿尘组(30只)和对照组(30只),铀矿尘组大鼠一次性非暴露气管内滴注20 mg/ml的粉尘悬液1 ml,对照组大鼠一次性气管内滴注生理盐水1 ml,分别于处理后7、14、21、30及60 d每组随机处死6只,取肺组织,HE染色观察肺组织形态学改变,天狼猩红染色法观察肺组织Ⅰ、Ⅲ型胶原变化,免疫组织化学法检测LN蛋白的表达.结果 铀矿尘致肺组织纤维化过程中可见Ⅰ、Ⅲ型胶原的大量增生,染尘后早期主要以Ⅰ型胶原增生为主.铀矿尘组21、30、60d时Ⅰ型、Ⅲ型胶原纤维面积百分比明显增高,与对照组比较,差异均有统计学意义(P<0.05或P<0.01).LN主要见于肺组织内血管、支气管周围、血窦壁以及肺间隔的基底膜,形态上以增粗的线状或丛状分布为主.铀矿尘组21、30、60 d时肺组织中LN阳性细胞积分吸光度(14.89±2.25、22.98±2.29、30.34±2.19)增加,与对照组(9.06±1.21、8.98±0.86、10.04±2.00)比较,差异有统计学意义(P<0.05,P<0.01).结论 铀矿尘诱导大鼠肺组织纤维化早期以Ⅰ型胶原纤维为主,后期Ⅰ型、Ⅲ型胶原纤维均大量增多,分布范围扩大.肺组织过程中有LN高表达.
目的 探討鈾礦塵緻大鼠纖維化過程中Ⅰ、Ⅲ型膠原、層粘連蛋白(Laminin,LN)錶達的變化特徵.方法 60隻Wistar大鼠隨機分為鈾礦塵組(30隻)和對照組(30隻),鈾礦塵組大鼠一次性非暴露氣管內滴註20 mg/ml的粉塵懸液1 ml,對照組大鼠一次性氣管內滴註生理鹽水1 ml,分彆于處理後7、14、21、30及60 d每組隨機處死6隻,取肺組織,HE染色觀察肺組織形態學改變,天狼猩紅染色法觀察肺組織Ⅰ、Ⅲ型膠原變化,免疫組織化學法檢測LN蛋白的錶達.結果 鈾礦塵緻肺組織纖維化過程中可見Ⅰ、Ⅲ型膠原的大量增生,染塵後早期主要以Ⅰ型膠原增生為主.鈾礦塵組21、30、60d時Ⅰ型、Ⅲ型膠原纖維麵積百分比明顯增高,與對照組比較,差異均有統計學意義(P<0.05或P<0.01).LN主要見于肺組織內血管、支氣管週圍、血竇壁以及肺間隔的基底膜,形態上以增粗的線狀或叢狀分佈為主.鈾礦塵組21、30、60 d時肺組織中LN暘性細胞積分吸光度(14.89±2.25、22.98±2.29、30.34±2.19)增加,與對照組(9.06±1.21、8.98±0.86、10.04±2.00)比較,差異有統計學意義(P<0.05,P<0.01).結論 鈾礦塵誘導大鼠肺組織纖維化早期以Ⅰ型膠原纖維為主,後期Ⅰ型、Ⅲ型膠原纖維均大量增多,分佈範圍擴大.肺組織過程中有LN高錶達.
목적 탐토유광진치대서섬유화과정중Ⅰ、Ⅲ형효원、층점련단백(Laminin,LN)표체적변화특정.방법 60지Wistar대서수궤분위유광진조(30지)화대조조(30지),유광진조대서일차성비폭로기관내적주20 mg/ml적분진현액1 ml,대조조대서일차성기관내적주생리염수1 ml,분별우처리후7、14、21、30급60 d매조수궤처사6지,취폐조직,HE염색관찰폐조직형태학개변,천랑성홍염색법관찰폐조직Ⅰ、Ⅲ형효원변화,면역조직화학법검측LN단백적표체.결과 유광진치폐조직섬유화과정중가견Ⅰ、Ⅲ형효원적대량증생,염진후조기주요이Ⅰ형효원증생위주.유광진조21、30、60d시Ⅰ형、Ⅲ형효원섬유면적백분비명현증고,여대조조비교,차이균유통계학의의(P<0.05혹P<0.01).LN주요견우폐조직내혈관、지기관주위、혈두벽이급폐간격적기저막,형태상이증조적선상혹총상분포위주.유광진조21、30、60 d시폐조직중LN양성세포적분흡광도(14.89±2.25、22.98±2.29、30.34±2.19)증가,여대조조(9.06±1.21、8.98±0.86、10.04±2.00)비교,차이유통계학의의(P<0.05,P<0.01).결론 유광진유도대서폐조직섬유화조기이Ⅰ형효원섬유위주,후기Ⅰ형、Ⅲ형효원섬유균대량증다,분포범위확대.폐조직과정중유LN고표체.
Objective To explore the characteristics of LN and type Ⅰ, Ⅲ collagen in pulmonary fibrosis induced by uranium ore dust in rats. Methods 60 adult Wistar rats were divided randomly into two groups, control group (30 rats)and uranium ore dust group (30 rats). Non-exposed intratracheal instillation method was used. Uranium ore dust group was exposed 20 mg/ml uranium ore dust suspension 1ml per rat,meanwhile control group was exposed normal saline 1ml per rat. Post-exposed the 7, 14, 21, 30 and 60 d, 6 rats in each group were killed randomly, lung tissue were collected. The pathological changes in lung tissue were observed by microscope using HE staining, the collagen Ⅰ and Ⅲ in lungs were observed by polarizing microscope using Biebrich scarlet staining. The expression of LN protein in lung tissue was observed by immunohistochemistry-SP. Results During lung fibrosis, a large amount of the proliferated Ⅰ and Ⅲ collagen in lungs were observed. Post-exposure to uranium ore dust, the characteristics in proliferated collagen in lungs were type Ⅰ collagen deposited in lung interstitium mainly in the early stage. The area percentage of collagen Ⅰ and Ⅲ was increased significantly at 7,14, 21, 30 and 60 d in the experimental group as compared with that in the control group (P<0.05 or P<0.01). The over expression of LN in the lung tissue were observed. The expression of LN was distributed in the lung tissue as thickening of the linear or cluster. The integral optical density of LN was increased significantly at 21,30 and 60d in the experimental group as compared with that in the control group(P<0.05 or P<0.01). Conclusions After exposure to uranium ore dust, the characteristics in proliferated collagen in lungs are the type of Ⅰ collagen deposited in lung interstitium mainly in the early stage, while the type of Ⅲ collagen increase significantly at the later period. The overexpression of LN exists in the process of pulmonary fibrosis. It suggests that LN has a role effect in the process of pulmonary fibrosis.