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机构地区:[1]南昌市第三医院中医科,江西南昌330009 [2]暨南大学附属第一医院妇产科,广东广州510632 [3]南昌市第三医院心内科,江西南昌330009
出 处:《中国病理生理杂志》2013年第4期615-618,共4页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.200025370)
摘 要:目的:观察麦冬抑制大鼠心肌成纤维细胞胶原合成的作用及其机制。方法:以培养的SD大鼠心肌成纤维细胞为观察对象,随机将心肌成纤维细胞分为4组(n=10):对照组(未用麦冬处理大鼠心肌成纤维细胞)、麦冬(10μg/L)组、麦冬(20μg/L)组和麦冬(30μg/L)组。测定不同组心肌成纤维细胞活力、[3H]-脯氨酸掺入率、TGF-β1、p-Smad2/3和Smad2/3蛋白表达的变化。结果:与对照组比较,麦冬(10μg/L)组大鼠心肌成纤维细胞活力、[3H]-脯氨酸掺入率、TGF-β1、p-Smad2/3和Smad2/3表达显著降低(P<0.01)。与麦冬(10μg/L)组比较,麦冬(20μg/L)组大鼠心肌成纤维细胞活力、[3H]-脯氨酸掺入率、TGF-β1、p-Smad2/3和Smad2/3表达显著降低(P<0.01)。与麦冬(20μg/L)组比较,麦冬(30μg/L)组大鼠心肌成纤维细胞活力、[3H]-脯氨酸掺入率、TGF-β1、p-Smad2/3和Smad2/3表达显著降低(P<0.01)。结论:麦冬对大鼠心肌纤维化有明显抑制作用,其机制可能与TGF-β1、p-Smad2/3和Smad2/3蛋白表达的降低有关。[ ABSTRACT] AIM: To investigate the inhibitory effect of Ophiopogon japonicus on rat cardiac fibroblast (CFs) and the underlying mechanism. METHODS: Cultured CFs from Sprague-Dawley (SD) rats were randomized into 4 groups: control group (normal rat cardiac fibroblasts), Ophiopogon japonicus of 10 μg/L group, Ophiopogon japonicus of 20 μg/L group and Ophiopogonjaponicus of 30 μg/L group. Cell vitality, [SH]-proline incorporation, and the protein ex- pression of TGF-β1-Smad2/3 and total Smad2/3 in CFs were determined. RESULTS: Compared with control, the cell vitality, [ 3H]-proline incorporation, and the protein expression of TGF-β1, p-Smad2/3 and total Smad2/3 were signifi- cantly decreased in Ophiopogon japonicus of 10 ug/L group. Compared with Ophiopogon japonicus of 10 ug/L group, the cell vitality, [ 3 HI-proline incorporation, and the protein expression of TGF-β1 , p-Smad2/3 and total Smad2/3 were signif- icantly decreased in Ophiopogon japonicus of 20 p^g/L group. Compared with Ophiopogon japonicus of 20 ~g/L group, the cell vitality, [ 3H ]-proline incorporation, and the protein expression of TGF-I3~ , p-Smad2/3 and total Smad2/3 were signifi- cantly decreased in Ophiopogon japonicus of 30 ug/L group. CONCLUSION: Ophiopogon japonicus may inhibit CFs. These actions are related to the changes of [ 3 H]-proline incorporation, and the protein expression of TGF-β1, p-Smad2/3 and total Smad2/3.
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