|
Abstract Objective To study the effects of calcium calmodulin dependent protein Kinase (CaMK) Ⅱon cardiac fi-broblast proliferation of rat and its mechanisms. Methods Cardiac fibroblasts cultured from neonatal SD rat were divid-ed into nine groups as follows:control group, Ang II (0.1μmol/L)group,Ang II+AIP (0.2μmol/L)group, Ang II+AIP (0.5μmol / L)group, AngⅡ+ AIP(1.0μmol / L)group, 10V1.0Hz EFS group, EFS +0.2 μmol / L AIP group, EFS +0.5μmol/L AIP group, EFS+1.0μmol/L AIP group. Cel counting and MTT were performed to detect cardiac fibroblasts proliferation. Protein expression of CaMKII-δB was measured by Western blot. mRNA expression of CaMK II- δB and CaMK II- δC was determined by RT-PCR. Results CaMKII inhibitor prevented cardiac fibroblasts proliferation in-duced by AngⅡor EFS(P<0.05)and inhibited expression of CaMKⅡδB and δC induced by Ang II(P<0.05). The ac-tivity of CaMKII increased when being exposed to Ang II for 24 hours(P<0.05)and more significantly for 48h(P<0.01). EFS enhanced CaMKII activation in a voltage-dependent manner with the voltage from 10V to 40V(P<0.05). Conclusion CaMKII inhibitor can prevent cardiac fibroblasts proliferation by inhibiting expression of CaMKⅡδB andδC.
|
|
|
|
|
|
