摘要
目的 :探讨血管紧张素 ( Ang )对心脏成纤维细胞 ( cfbs)胶原代谢和分裂增殖的直接影响。方法 :培养 SD大鼠乳鼠 cfbs,测定其胶原合成总量、 型胶原含量及胶原酶活力 ;检测细胞增殖核抗原 ( PCNA)及与增殖相关的 c- m yc基因的表达。结果 :在一定浓度和作用时间下 ,Ang 能显著增加培养细胞胶原合成总量及 型胶原合成量 ;10 - 9～ 10 - 7m ol/ L Ang 均可在 2 4 h后使培养细胞分泌的前胶原酶活性受到抑制 ,Ang 的此种作用可被 saralasin拮抗 ;10 - 8m ol/ L 的 Ang 不促进 PCNA蛋白及 c- m yc基因的表达。结论 :一定浓度和时间作用下 ,Ang 能不同程度地促进胶原合成 ,抑制胶原酶活力 ,使胶原沉积的净效应增加 ,从而加速心肌纤维化。但是Ang 在体外不能促进
Objective: To explore the influence of angiotensin Ⅱ(AngⅡ) on cardiac fibroblasts (cfbs) collagen synthesis as well as the activity of precollagenase secreted by cfbs and to clarify whether AngⅡ was mitogenic in cultured cfbs.Method: Sirus Red method was employed to evaluate cultured cardiac fibroblasts collagen synthesis;type Ⅰ collagen was measured by competitive ELISA; collagenase activity was tested by fluorescence spectrophotometry. Immunohistochemical method was employed to evaluate the manifestation of proliferative cellular nuclear antigen (PCNA) and c myc, the proliferation related gene, transcription level were tested by in situ hybridization.Result: At the doses of 10 -9 ～10 -7 mol/L, AngⅡ could enhance gross collagen production in both 24 h and 48 h and type Ⅰ collagen in medium in 24 h in a dose dependent manner.Collagenase activity decreased with concentration of AngⅡ increasing. These effects of AngⅡ could be completely abolished by its receptor antagonist, saralasin. AngⅡ did not increase PCNA expression and c myc gene transcription.Conclusion: AngⅡ enhances collagen synthesis of cardiac fibroblasts and inhibites collagenase activity, thus increasing net collagen accumulation and accelerating cardiac fibrosis. AngⅡ has no direct effect on cardiac fibroblasts proliferation in vitro.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2001年第7期318-320,共3页
Journal of Clinical Cardiology
