Beneficial effects of intramyocardial mesenchymal stem cells and VEGF 165 plasmid injection in rats with furazolidone induced dilated cardiomyopathy

To explore the impact of myocardial injection of mesenchymal stem cells ( MSC s) and specific recombinant human VEGF 165 ( hVEGF 165 ) plasmid on collagen remodelling in rats with furazolidone induced dilated cardiomyopathy ( DCM ). DCM was induced by furazolidone (0.3 mg/bodyweight (g)/day per gavage for 8 weeks). Rats were then divided into four groups: ( i ) PBS group ( n  = 18): rats received equal volume myocardial PBS injection; ( ii ) MSC s group ( n  = 17): 100 μl culture medium containing 10 5 MSC s were injected into four sites of left ventricular free wall (25 μl per site); ( iii ) GENE group ( n  = 18): pCMV en‐ MLC 2v‐ EGFP ‐ VEGF 165 plasmid [5 × 109 pfu (0.2 ml)] were injected into four sites of left ventricular free wall (0.05 ml per site)] and ( iv ) MSC s+ GENE group ( n  = 17): rats received both myocardial MSC s and pCMV en‐ MLC 2v‐ EGFP ‐ VEGF 165 plasmid injections. After 4 weeks, cardiac function was evaluated by echocardiography. Myocardial mRNA expressions of type I, type III collagen and transforming growth factor ( TGF )‐β1 were detected by RT ‐ PCR . The protein expression of hVEGF 165 was determined by Western blot. Myocardial protein expression of hVEGF 165 was demonstrated in GENE and MSC s+ GENE groups. Cardiac function was improved in MSC s, GENE and MSC s+ GENE groups. Collagen volume fraction was significantly reduced and myocardial TGF ‐β1 mRNA expression significantly down‐regulated in both GENE and MSC s+ GENE groups, collagen type I/III ratio reduction was more significant in MSC s+ GENE group than in MSC s or GENE group. Myocardial MSC s and hVEGF 165 plasmid injection improves cardiac function possibly through down‐regulating myocardial TGF ‐β1 expression and reducing the type I/III collagen ratio in this DCM rat model.