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甲状腺素对血管紧张素Ⅱ所致心肌成纤维细胞胶原合成改变的影响 被引量:3

Effect of Thyroid Hormone on the Changes of Collagen Synthesis in Cardiac Fibroblasts Induced by Angiotension Ⅱ
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摘要 目的 :以AngⅡ处理培养的心肌成纤维细胞 ,促使细胞中胶原的合成发生改变 ,观测T3对AngⅡ所致细胞胶原合成改变的影响。方法 :以AngⅡ及T3分别或同时作用于培养的大鼠心肌成纤维细胞 ,通过测定3H TdR和3H Leu掺入来了解成纤维细胞增殖率和蛋白质合成率 ,同时用免疫细胞化学方法检测成纤维细胞中Ⅰ、Ⅲ型胶原的表达。结果 :AngⅡ使成纤维细胞3H TdR和3H Leu掺入增加 ,同时细胞中Ⅰ、Ⅲ型胶原的表达也显著增加。T3组成纤维细胞3H TdR和3H Leu掺入虽然也增加 ,但T3组细胞中Ⅰ、Ⅲ型胶原的表达却呈显著性降低。当T3与AngⅡ共同作用于成纤维细胞时 ,与T3组和AngⅡ组比较 ,3H TdR和3H Leu的掺入率没有发生显著性的变化 ;与AngⅡ组比较 ,细胞中Ⅰ、Ⅲ型胶原的表达显著性降低 ,与对照组的表达一致。结论 :T3能降低AngⅡ所致的心肌成纤维细胞中Ⅰ。 Objective:To add angiotensin Ⅱto the culture medium of cardiac fibroblast to promot it prolifering and its collagen synthesizing, and studying the effect of thyroid hormone on the changes of collagen synthesis in fibroblasts induced by AngⅡ. Methods: Cardicac fibroblasts were cultured using AngⅡ and T 3 respectively or synchronously. The rates of fibroblast proliferation and protein synthesis were measured by assaying the incorporation rates of 3H TdR and 3H Leu respectively. The expressions of collagenⅠand Ⅲwere detected by the immunocytochemical method. Results: AngⅡ significantly increased the 3H TdR and 3H Leu incorporation rates in fibroblasts. The expressions of collagenⅠand Ⅲ were increased, too. Though T 3 could increase the 3H TdR and 3H Leu incorporation rates in fibroblasts significantly, the expressions of collagenⅠand Ⅲ were decreased in the condition of T 3 compared with control group. When both T 3 and AngⅡwere added in the culture medium, the 3H TdR and 3H Leu incorporation rates didn't change compared with T 3 group and AngⅡgroup. But compared with AngⅡgroup, the expressions of collagenⅠand Ⅲ were significantly decreased. Their expressions is the same as the control group. Conclusion:It suggested that T 3 could decrease the increase of collagen synthesis in cardiac fibroblasts induced by AngⅡ.
出处 《武汉大学学报(医学版)》 CAS 2002年第1期1-4,共4页 Medical Journal of Wuhan University
基金 湖北省自然科学基金 (980 91)
关键词 心肌 成纤维细胞 甲状腺素 血管紧张素Ⅱ 合成 影响 myocardium fibroblasts thyroxine angiotensin Ⅱ collagen
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