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GW24-e1172 Fasudil restrain atrial fibrosis and its mechanism in a rat model of type 2 diabetes
  1. Jinling Chen,
  2. Yongquan Wu
  1. Beijing Friendship Hospital, Capital Medical University

Abstract

Objectives This study was to investigate the role of RhoA/Rho kinase (ROCK) in atrial fibrosis in diabetic hearts, and the effects of fasudil hydrochloride hydrate on atrial fibrosis.

Methods A 8-week-old female Sprague-Dawley rat model of type 2 diabetes was established using high fat diet combined with streptozotocin (30 mg/kg, once, ip). Animals were randomly divided into 3 groups: control rats, untreated diabetic rats which received vehicle and treated diabetic rats that received Rho kinase inhibitor fasudil hydrochloride hydrate (10 mg·kg-1·d-1, ip, for 14 weeks). The morphological features of atrial fibrosis were observed using Masson staining. The mRNA expression of RhoA, ROCK-I, ROCK-II, type-I and type-III procollagen were assessed with RT-PCR. The protein levels of RhoA, ROCK-I, ROCK-II were evaluated using Western blotting.

Results The atria of untreated diabetic rats showed remarkable atrial fibrosis as compared to the control rats, the mRNA expression levels of type-I and type-III procollagen were increased, the mRNA and protein expression levels of RhoA, ROCK-I, ROCK-II were upregulated. The treatment with fasudil hydrochloride hydrate significantly relieved atrial fibrosis, the mRNA expression levels of type-I and type-III procollagen were reduced, the mRNA and protein expression levels of RhoA, ROCK-I, ROCK-II were decreased.

Conclusions The data suggest that RhoA/ROCK is involved in atrial fibrosis and fasudil hydrochloride hydrate ameliorates atrial fibrosis in rats with type 2 diabetes.

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