| Background: Atrial ifbrillation (AF) is the most commonly encountered arrhythmiain adults and can increase the risk of premature death. Experimental data from animalmodels of AF show that AF is associated with progressive atrial ifbrosis. Diabetesmellitus promotes atrial structural remodeling，which produced atrialarrhythmogenicity. So，we could conifrm that diabetes mellitus lead to Atrialifbrillation through atrial ifbrosis. While the mechanism of atrial ifbrosis is not veryclear. This study was to investigate the role of RhoA/Rho kinase(ROCK) in atrialifbrosis in diabetic hearts, and the effects of fasudil hydrochloride hydrate on atrialfibrosis.Methods: A8-week-old female Sprague-Dawley rat model of high glucose wasestablished using high fat diet combined with streptozotocin (30mg/kg，once，ip).Animals were randomly divided into3groups: control rats, untreated high glucoserats which received vehicle and treated high glucose rats that received Rho kinaseinhibitor fasudil hydrochloride hydrate (10mg.kg-l.d-l，ip, for14weeks). Themorphological features of atrial ifbrosis were observed using Masson staining. ThemRNA expression of RhoA，ROCK-I，ROCK-II，type-I and type-Ill procollagen wereassessed with RT-PCR. The protein levels of RhoA, ROCK-I, ROCK-II wereevaluated using Western blotting.Results: The atria of untreated high glucose rats showed remarkable atrial ifbrosis ascompared to the control rats, the mRNA expression levels of type-I and type-Illprocollagen were increased, the mRNA and protein expression levels of RhoA, ROCK-I, ROCK-II were upregulated. The treatment with fasudil hydrochloridehydrate signiifcantly relieved atrial ifbrosis，the mRNA expression levels of type-Iand type-Ill procollagen were reduced, the mRNA and protein expression levels ofRhoA, ROCK-I，ROCK-II were decreased.Conclusion: The data suggest that RhoA/ROCK is involved in atrial ifbrosis andfasudil hydrochloride hydrate ameliorates atrial ifbrosis in high glucose rats. |
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