蛋白激酶C对大鼠逼尿肌肌条收缩活动影响的实验研究

Effect of protein kinase C on contractile activity of detrusor strips in rats

目的探讨蛋白激酶C对大鼠离体逼尿肌肌条自发收缩活动的影响。方法建立逼尿肌不稳定(detrusor instability,DI)大鼠模型,制做大鼠逼尿肌肌条,观察不同浓度(3×10^(-7)～3×10^(-4))mol/L的PMA和H-7对DI及逼尿肌稳定(detrusor stability,DS)大鼠逼尿肌肌条自发收缩活动的影响。结果 3×10^(-7)～3×10^(-6)mol/L的PMA可明显增加DI、DS大鼠逼尿肌肌条自发收缩频率及收缩幅度,且DI组收缩频率高于DS组(P<0.05),但(3×10^(-5)～3 × 10^(-4))mol/L的PMA对DI、DS大鼠逼尿肌肌条自发收缩频率和收缩幅度的促进作用无统计学差别(P>0.05)。H-7能逆转PMA诱发的DS肌条的收缩作用,可明显抑制DI肌条自发收缩频率(P<0.05),但对其收缩幅度无影响(P>0.05)。结论蛋白激酶C信号通路可能介导了DI逼尿肌自发兴奋性增高的细胞内信号转导过程。

Objective To study the effect of protein kinase C （PKC）on the contractile activity of isolated detrusor strips in rats. Methods A rat model of detrusor instability （DI） was developed for detrusor strips before the effect of different concentrations （3 ×10^-7-3×10^-4） of mol/LPKC activator PMA and inhibitor H -7 on the contractility in DI and detrusor stability （DS） rats was observed. Results PMA （3 ×10^-7-3×10^-6）mo[/L significantly increased the range and frequency of detrusor automatic contractility＂ in DI and DS rats,and the frequency in DI group rats was significantly higher than that in DS group （P 〈 0. 01 ,P 〈 0.05）, but no significant difference was observed in the range and frequency of automatic contractility in DS and DI rats by（3×10^-5-3×10^-4 ） mol/L PMA treatment （P 〉 0.05）. H-7 reversed the detrusor automatic contractility in DS rats induced by PMA and inhibited the frequency of automatic contractility in DI rats （ P 〈 0.05 ）, but without any effect on the range of contractility （ P 〉 0.05 ）. Conclusions PKC signal path- ways might mediate the intracellular signal transduction process of the increase of detrusor excitability in DI rats.