MicroRNAs (miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7, and also in a murine heart failure model, implying that miR-30b might play an important role in heart diseases. To study miR-30b in vivo function, we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain (α-MHC). qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice (P < 0.05). miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure. At present, little is known about how miR-30b regulates myocardial infarction. We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls. Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion, these transgenic mice had lower releases of LDH, CK and cTnⅠ(P < 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P < 0.05). Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice. In conclusion, miR-30b has protective effect upon ischemic-reperfusion injury. And it may provide a new therapeutic approach for preventing and treating myocardial infarction.