Role Of MiRNA-133a In Myocardial Sevoflurane Postconditioning

Objective:To evaluate the effect of sevoflurane postconditioning on ischemia reperfusion injury in C57 rats and the role of mi RNA-133 a. Methods: Thirty C57 rats were equally randomized to three groups: Control group, where the rats were treated with thoracotomy only; IR group, where the rats were treated with ischemia for 30 min and reperfusion for 180 min; Sevo+I/R group, where the rats were treated with 2.4% sevoflurane for 15 min before reperfusion. The extent of myocardial infarction, LDH and CK activities were measured immediately after treatment. The myocardial tissue was collected after IR to evaluate the mi RNAs expression level by mi RNA-microarray and quantitative real-time RT-PCR. Realtime PCR was conducted to identify changes in m RNA expression of apoptosis-related genes such as Bcl-2, Bax and Caspase-9(CASP9), and Western blot was used to compare the protein expression level of CASP9 in the three groups. Results: sevoflurane reduced the IR-induced infarct size of the left ventricle, and decreased CK and LDH levels(P<0.05). Mi RNA-microarray and RT-PCR showed that myocardial-specific mi RNA-133 a was down-regulated by IR, and up-regulated by IPost compared with IR(P<0.05). Furthermore, sevoflurane up-regulated the m RNA expression of Bcl-2, down-regulated that of Bax and CASP9(P<0.05). Western blot showed that IPost also down-regulated the CASP9 protein expression compared with IR(P<0.05). Conclusion:Mi RNAs are associated with the protective effect of Sevoflurane against myocardial IR injury. Sevoflurane can upregulate mi RNA-133 a. Myocardial-specific and mi RNA-133 a may play an important role in sevoflurane protection by regulating apoptosis-related genes.