The effect of thymosin beta 4 plasmid in myocardial infarction
OBJECTIVE: Our previous study employing a rat heterotopic abdominal heart transplantation model (Ono-Lindsey method) showed that significantly less myocardial scar tissue was formed in both the Tb4 plasmid and Tb4 peptide groups compared to controls. In the present study, myocardial infarction was induced in the normal working rat heart and the effect of the Tb4 plasmid on myocardial scar formation was examined. MATERIALS & METHODS: The left anterior descending branches of the left coronary artery of rats were ligated to induce broad antero septal myocardial infarction. Rats were divided into the following 2 groups: Tb4 plasmid (50 μg/50 μl) group and empty vector injection control group. In each group, the drug was injected at 2 or 3 sites in the myocardial infarct area. Myocardial tissue, harvested 4 weeks later, was evaluated using Masson trichrome staining, and the myocardial scar volume was measured. In addition, expression of the plasmid at the local myocardium was detected in the plasmid group 1 week later by immunostaining. RESULTS: The immunostain revealed Tb4 expression in the myocardial infarct area where the Tb4 plasmid had been injected. Myocardial scar volume was significantly lower in the Tb4 plasmid group (19.5±4.6%, n ＝21, p ＝0.019 vs control) than in the control group (23.4±4.7%, n ＝15). CONCLUSION: Significantly less myocardial scar tissue was formed in the Tb4 plasmid group compared with the control group. The Tb4 plasmid can reduce myocardial scar volume in myocardial infarction by means of the expression of Tb4. (Accepted on June 3, 2011)
