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目的 :探讨一氧化氮 (NO )对内皮素 (ET)促大鼠培养心肌细胞肥大及肌球蛋白重链 (MHC)基因表达的影响。方法 :对 12 0只大鼠采用心肌细胞培养及斑点杂交的方法 ,同时测定心肌细胞直径、数目及 3H-亮氨酸(3H- L eu)掺入率。结果 :NO组、ET组心肌细胞数目与对照组比较 ,均无明显差异 (P >0 .0 5 ) ,ET组细胞直径较对照组增加 (34 .5± 5 .5 ) % (P <0 .0 1) ,NO组较对照组增加 (6 .2± 2 .5 ) % (P >0 .0 5 ) ;NO明显抑制 ET促 3H-L eu掺入率的增加 (P <0 .0 1) ,NO组与对照组相比 ,β- MHC m RNA表达明显增加 ,α- MHC m RNA表达明显减少 (P <0 .0 1) ,NO显著逆转 ET的上述作用。结论 :NO有抑制 ET促心肌细胞肥大的作用 ,并可逆转 ET致MHC同工蛋白的病理性转换
Objective: To investigate the effect of nitric oxide (NO) on cardiomyocyte hypertrophy and myosin heavy chain (MHC) gene expression induced by endothelin (ET) in rats. Methods: The diameter and number of cardiomyocytes and the incorporation of 3H-L eu were determined by cardiomyocyte culture and dot blot hybridization in 120 rats. Results: Compared with the control group, the number of cardiomyocytes in NO group and ET group showed no significant difference (P> 0.05), the diameter of ET group increased (34.5 ± 5.5)% (P <0) .0 1), NO increased (6.2 ± 2.5)% (P> 0.05) in NO group compared with control group; NO significantly inhibited the increase of ET-3H-L eu incorporation 1). Compared with the control group, the expression of β-MHC m RNA and the expression of α-MHC m RNA in NO group were significantly decreased (P <0.01). NO significantly reversed the above effects of ET. CONCLUSION: NO inhibits ET-induced cardiomyocyte hypertrophy and reverses the pathological conversion of ET-induced MHC isoenzyme