中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2011年
7期
909-911,916
,共4页
缬氨酸/类似物和衍生物/药理学%呼吸窘迫综合征,成人/代谢%转化生长因子β/生物合成%Smad蛋白质类/生物合成%肺/损伤/代谢
纈氨痠/類似物和衍生物/藥理學%呼吸窘迫綜閤徵,成人/代謝%轉化生長因子β/生物閤成%Smad蛋白質類/生物閤成%肺/損傷/代謝
힐안산/유사물화연생물/약이학%호흡군박종합정,성인/대사%전화생장인자β/생물합성%Smad단백질류/생물합성%폐/손상/대사
Valine/AA/PD%Respiratory distress syndrome,adult/ME%Transforming growth factor beta/BI%Smad proteins/BI%Lung/IN/ME
目的 观察缬沙坦对急性肺损伤大鼠TGF-β/Smad信号通路的影响.方法 24只SD雄性大鼠随机分为对照组、模型组和缬沙坦组三组,每组8只.缬沙坦组于气管内滴注博莱霉素(BLM)生理盐水溶液(5 mg/kg)以复制急性肺损伤动物模型,并于造模当天每日给予缬沙坦(20mg/kg)灌胃;模型组以生理盐水代替缬沙坦灌胃;对照组则均用生理盐水代替BLM和缬沙坦.各组动物均于制模开始后第7天处死,分取肺组织行病理切片HE染色观察肺损伤程度、免疫组化技术检测肺组织TGF-β1、Smad2/3和Smad7蛋白的表达水平.结果 缬沙坦组大鼠肺组织损伤程度较模型组比较明显减少(P＜0.01).模型组肺组织内TGF-β1、Smad2/3蛋白表达水平较对照组明显增强(P＜0.01).缬沙坦组TGF-β1、Smad2/3蛋白表达水平较模型组降低(P＜0.01).Smad7蛋白在模型组肺组织内表达明显低于对照组(0.23±0.02 vs 0.36±0.03,P＜0.01),缬沙坦组Smad7蛋白表达同模型组比较明显增强(P＜0.01).结论 缬沙坦可下调急性肺损伤大鼠肺组织内TGF-β1、Smad2/3蛋白表达,上调Smacd7蛋白表达,从而阻断TGF-β/Smad信号通路,减轻急性肺损伤程度.
目的 觀察纈沙坦對急性肺損傷大鼠TGF-β/Smad信號通路的影響.方法 24隻SD雄性大鼠隨機分為對照組、模型組和纈沙坦組三組,每組8隻.纈沙坦組于氣管內滴註博萊黴素(BLM)生理鹽水溶液(5 mg/kg)以複製急性肺損傷動物模型,併于造模噹天每日給予纈沙坦(20mg/kg)灌胃;模型組以生理鹽水代替纈沙坦灌胃;對照組則均用生理鹽水代替BLM和纈沙坦.各組動物均于製模開始後第7天處死,分取肺組織行病理切片HE染色觀察肺損傷程度、免疫組化技術檢測肺組織TGF-β1、Smad2/3和Smad7蛋白的錶達水平.結果 纈沙坦組大鼠肺組織損傷程度較模型組比較明顯減少(P＜0.01).模型組肺組織內TGF-β1、Smad2/3蛋白錶達水平較對照組明顯增彊(P＜0.01).纈沙坦組TGF-β1、Smad2/3蛋白錶達水平較模型組降低(P＜0.01).Smad7蛋白在模型組肺組織內錶達明顯低于對照組(0.23±0.02 vs 0.36±0.03,P＜0.01),纈沙坦組Smad7蛋白錶達同模型組比較明顯增彊(P＜0.01).結論 纈沙坦可下調急性肺損傷大鼠肺組織內TGF-β1、Smad2/3蛋白錶達,上調Smacd7蛋白錶達,從而阻斷TGF-β/Smad信號通路,減輕急性肺損傷程度.
목적 관찰힐사탄대급성폐손상대서TGF-β/Smad신호통로적영향.방법 24지SD웅성대서수궤분위대조조、모형조화힐사탄조삼조,매조8지.힐사탄조우기관내적주박래매소(BLM)생리염수용액(5 mg/kg)이복제급성폐손상동물모형,병우조모당천매일급여힐사탄(20mg/kg)관위;모형조이생리염수대체힐사탄관위;대조조칙균용생리염수대체BLM화힐사탄.각조동물균우제모개시후제7천처사,분취폐조직행병리절편HE염색관찰폐손상정도、면역조화기술검측폐조직TGF-β1、Smad2/3화Smad7단백적표체수평.결과 힐사탄조대서폐조직손상정도교모형조비교명현감소(P＜0.01).모형조폐조직내TGF-β1、Smad2/3단백표체수평교대조조명현증강(P＜0.01).힐사탄조TGF-β1、Smad2/3단백표체수평교모형조강저(P＜0.01).Smad7단백재모형조폐조직내표체명현저우대조조(0.23±0.02 vs 0.36±0.03,P＜0.01),힐사탄조Smad7단백표체동모형조비교명현증강(P＜0.01).결론 힐사탄가하조급성폐손상대서폐조직내TGF-β1、Smad2/3단백표체,상조Smacd7단백표체,종이조단TGF-β/Smad신호통로,감경급성폐손상정도.
Objective To observe the effect of Valsartan on a rat model of acute lung injury and the expression of transforming growth factor-β,TGF-β) ,Smad2/3, Smad7. Methods Twenty-four male adult Sprague-Dawley rats were random divided into three groups : The bleomycin (BLM) group, the control group, and the Valsartan group. Each group contained eight rats. The Valsartan group was treated with Valsartan everyday at a dose of 20 mg/kg after a single intratracheal instillation of bleomycin at a dose of 5mg/kg. BLM group was treated with saline instead of Valsartan after an instillation of bleomycin. The control group was treated with saline instead of Valsartan and bleomycin. Each group was killed at the 7th day after instillation. The lung tissues were harvested for H. E. stain, the immunohistochemistry was used to detect the expressions of TGF-β1, Smad2/3 ,and Smad7. Results The degree of alveolitis in the Valsartan group was ameliorated, compared with those in BLM group (P ＜0. 01). The expressions of TGF-β1 and Smad2/3 in lung tissue of the Valsartan group were significantly lower than that of BLM group(P ＜0. 01). The expressions of Smad7 in lung tissue of the Valsartan group were significantly higher than that of BLM group (0.23 ±0. 02 vs0. 36 ±0.03, P ＜0.01). Conclusions Valsartan could alleviate acute lung injury in rats, which probably be due to the expression decrease of TGF-β1 and Smad2/3 and the expression increase of Smad7 in lung tissues.
