科研之友
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摘要
Objective: To explore the association between collagen cross-linking (CCL) and cardiac function in rats with furazolidone induced dilated cardiomyopathy (DCM). Methods and results: Forty 2-week-old Sprague-Dawlay (SD) rats were used, 30 rats were treated with furazolidone (0.15 mg/body weight (g)/day per gavage for 8 weeks, FZ group), 10 rats were treated by equal volume water daily per gavage for 8 weeks (Control group, CON). After 8 weeks, survival rate was 100% in CON group and 73.33% in FZ group (22/30, P<0.05). Echocardiography revealed that both left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly reduced, while left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) were significantly increased (P<0.001) in FZ rats compared to CON rats. Body weight was significantly decreased while heart weight/body weight ratio was significantly increased in FZ group (both P<0.05). Collagen volume fraction (16.39%+/- 2.06% versus 2.78 +/- 1.10%, P<0.001) and the degree of CCL (6.13 +/- 0.96 versus 5.18 +/- 0.12, P<0.05) were significantly increased in FZ group than in CON group. mRNA expression of myocardial collagen I, collagen III, N2B and LOX were significantly upregulated, while mRNA expression of titin and N2BA were significantly down-regulated in FZ group compared with CON group (all P<0.05). Moreover, CCL was negatively correlated with LVEF and LVFS while positively correlated with LVEDD and LVESD in FZ group. Conclusion: Increased collagen cross-linking is linked with reduced left ventricular dysfunction and aggravated left ventricular remodeling in this FZ-induced DCM rat model.
