升主动脉缩窄心衰大鼠心肌PKC活性测定

The role of protein kinase C in the transition from cardiac hypertrophy to failure induced by ascending aortic banding in rats

目的 探讨升主动脉缩窄慢性压力后负荷心肌肥厚转变为心力衰竭过程中心肌蛋白激酶C(PKC)比活性的变化及意义。方法 用泰夫隆管环扎幼鼠升主动脉 ,制作慢性压力后负荷心肌肥厚 心力衰竭模型。据改良Takai放射性核素酶解测定法 ,应用γ 32 P ATP测定不同病理时期心肌组织中PKC比活性。结果 与假手术组比较 ,肥厚组心肌胞膜、胞浆PKC比活性明显增高 (P <0 0 1)、PKC膜 /浆比值明显增加 (P <0 0 1) ;心力衰竭组心肌胞膜、胞浆PKC比活性差异均无显著性(P >0 0 5 ) ,但PKC膜 /浆比值明显增加 (P <0 0 1)。结论 PKC亚细胞水平的活性变化在慢性压力后负荷心肌肥厚

Objective To evaluate protein kinase C (PKC) activity and its contribution in the transition from pressure overload hypertrophy(POH) to congestive heart failure (CHF) Methods Rat model of pressure overload heart failure was induced by ascending aorta banding of young Wistar rats PKC activity was determined by measuring the incorporation of 32 P from γ 32 P ATP into protamine Results Compared with sham operated groups, in the CHF group, 12 weeks after operation, heart weight (HW) and HW/body weight (BW) increased 71 3% and 69 5%, respectively, with normal±dp/dt max ( P >0 05); 20 weeks later, HW and HW/BW were 80% and 94% higher, respectively( P <0 01), with decreased ±dp/dt max ( P <0 01) In POH group, PKC activity increased greatly in membrane fraction( P =0 01) with slightly higher cytosol PKC activity ( P <0 05). The ratio of membrane/cytosol(M/C) increased significantly( P <0 001) while neither membrane nor cytosol showed significant change in CHF group( P >0 05), but the M/C increased ( P <0 01) Conclusions The activity of PKC was constantly activated in these two pathological stages PKC was activated in an escalating manner in POH These data indicate that PKC might play a key regulatory role in the development of pressure overload heart failure