Abstract
Background Myocardial brosis is closely associated with cardiac dysfunction, arrhythmia and sudden cardiac death. A model of myocardial fibrosis induced by isoprenaline was used to determine the in uence of exogenous adiponectin on myocardial brosis. Methods Thirty mice were equally and randomly divided into three groups: isoproterenol (ISO, n=10), adiponectin and isoproterenol (APN+ISO, n=10) and sham (n=10). Isoproterenol (7.5 mg/kg/day) was injected intraperitoneally (i.p.) in the ISO group and APN+ISO group for 3 consecutive days to establish a model of myocardial brosis; normal saline was injected in the sham group. From day 4, adiponectin was injected (10 μg/kg/day; i.p.) in the APN+ISO group for 32 days; normal saline was injected in ISO and sham groups for 32 days. Five weeks later, mice were sacri ced and myocardial tissue was dyed by Sirius Red to observe the collagen morphology. The collagen volume fraction (CVF) was calculated. Protein and mRNA expression of type-I and type-III collagen in the myocardium was detected by RT- PCR and western blotting respectively. Results Type-I collagen in myocardial interstitial tissue was significantly increased in the ISO group. Collagen in myocardial interstitial tissue in the ISO+APN group was decreased signi cantly compared with the ISO group. Expression of type-I collagen mRNA in ISO and ISO+APN groups was signi cantly higher than that in the sham group (3.01±0.78, 2.32±0.82 vs 1, respectively; P<0.01). Expression of type-I collagen mRNA in the ISO+APN group was significantly lower than that in the ISO group (2.32±0.82 vs 3.01±0.78, respectively; P<0.01). Expression of type-III collagen mRNA in the ISO group and ISO+APN group was signi cantly higher than that in the sham group (2.39±0.70, 1.62±0.57 vs 1, respectively; P<0.01). Expression of type-III collagen mRNA in the ISO+APN group was signi cantly lower than that in the ISO group (1.62±0.57 vs 2.39±0.70, respectively; P<0.01). Expression of type-I collagen protein in the myocardium in the ISO+APN group was signi cantly higher than that in the sham group (0.73±0.19 vs 0.28±0.15, respectively; P<0.001), but it was signi cantly lower than the expression of type-I collagen protein in the ISO group (0.53±0.17 vs 0.73±0.19, respectively; P<0.001). Conclusions Supplementation with exogenous adiponectin can inhibit myocardial fibrosis induced by isoproterenol.
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