论文部分内容阅读
目的 探讨细胞骨架在牵张刺激心肌细胞肥大过程中的作用。方法 在可变形膜上培养心肌细胞 ,采用 3H 亮氨酸掺入法反映心肌细胞肥大指标和放射免疫测定培养上清血管紧张素Ⅱ和内皮素的含量 ,观察细胞骨架解聚剂对牵张刺激心肌细胞肥大的影响。结果 4μmol/L秋水仙素即可部分地抑制牵张刺激诱导的3H 亮氨酸掺入 (P <0 .0 5 ) ,而细胞松驰素B对牵张刺激诱导的 3H 亮氨酸掺入无影响。牵张刺激细胞骨架解聚剂处理后的培养上清刺激心肌细胞 3H 亮氨酸掺入的活性显著低于单纯牵张刺激时的培养基。同时 ,细胞骨架解聚剂显著抑制牵张刺激心肌细胞分泌血管紧张素Ⅱ和内皮素。结论 细胞骨架仅通过介导细胞自分泌细胞生长因子参与牵张刺激诱导的心肌细胞肥大反应。
Objective To investigate the role of cytoskeleton in stretch-induced cardiomyocyte hypertrophy. Methods Myocardial cells were cultured on deformable membrane. 3H-leucine incorporation method was used to detect the cardiomyocyte hypertrophy index and the content of angiotensin Ⅱ and endothelin in the culture supernatant by radioimmunoassay. The effect of cytoskeletal depolymerization on stretch- Effects of hypertrophy on cardiomyocytes. Results 4μmol / L colchicine could partially inhibit stretch-induced incorporation of 3H-leucine (P <0.05), while cytochalasin B induced stretch-induced 3H-leucine incorporation no effect. Stretch cytosolic cytosolic protoporphyrin treatment of cultured supernatant to stimulate myocardial 3H-leucine incorporation activity was significantly lower than the simple stretch stimulation medium. At the same time, cytoskeletal depolymerization significantly inhibited the stretch and stimulated cardiomyocytes to secrete angiotensin Ⅱ and endothelin. Conclusion Cytoskeleton can only mediate stretch-induced cardiomyocyte hypertrophy through mediating cell autocrine growth factor.