Role of XXXX and @entity34513 in @entity741 postconditioning.

@entity1976 @entity63 @entity2310 @entity34512 @entity2311 @entity1188 @entity741 @entity35 @entity583 @entity34513
BACKGROUND: Ischemic postconditioning (IPost) has aroused much attention since 2003 when it was firstly reported. The role of microRNAs (miRNAs or miRs) in IPost has rarely been reported. The present study was undertaken to investigate whether miRNAs were involved in the protective effect of IPost against @entity741 -reperfusion (IR) injury and the probable mechanisms involved. METHODS: Thirty SD @entity35 weighing 250-300 g were equally randomized to three groups: Control group, where the @entity35 were treated with thoracotomy only; IR group, where the @entity35 were treated with @entity63 for 60 min and reperfusion for 180 min; and IPost group, where the @entity35 were treated with 3 cycles of transient IR just before reperfusion. The extent of @entity583 , LDH and CK activities were measured immediately after treatment. Myocardial apoptosis was detected by TUNEL assay. The myocardial tissue was collected after IR or IPost stimulation to evaluate the miRNAs expression level by miRNA-microarray and quantitative real-time RT-PCR. Real-time PCR was conducted to identify changes in mRNA expression of apoptosis-related genes such as @entity1976 , @entity2310 and @entity2311 ( @entity2311 ), and Western blot was used to compare the protein expression level of @entity2311 in the three groups. The miRNA mimics and anti-miRNA oligonucleotides (AMO) were transferred into the cultured neonatal cardiomyocytes and myocardium before they were treated with IR. The effect of miRNAs on apoptosis was determined by flow cytometry and TUNEL assay. @entity2311 , as one of the candidate target of @entity34513 , was compared during IR after the @entity34513 mimic or AMO-133a was transferred into the myocardium. RESULTS: IPost reduced the IR-induced @entity1188 size of the left ventricle, and decreased CK and LDH levels. TUNEL assay showed that myocardial apoptosis was attenuated by IPost compared with IR. MiRNA-microarray and RT-PCR showed that myocardial-specific @entity34512 and @entity34513 were down-regulated by IR, and up-regulated by IPost compared with IR. Furthermore, IPost up-regulated the mRNA expression of @entity1976 , down-regulated that of @entity2310 and @entity2311 . Western blot showed that IPost also down-regulated the @entity2311 protein expression compared with IR. The results of flow cytometry and TUNEL assay showed that up-regulation of @entity34512 and @entity34513 decreased apoptosis of cardiomyocytes. @entity34513 mimic down-regulated @entity2311 protein expression and attenuated IR-induced apoptosis. CONCLUSION: MiRNAs are associated with the protective effect of IPost against @entity741 . IPost can up-regulate @entity34512 and @entity34513 , and decrease apoptosis of cardiomyocyte. Myocardial-specific @entity34512 and @entity34513 may play an important role in IPost protection by regulating apoptosis-related genes. @entity34513 may attenuate apoptosis of myocardiocytes by targeting @entity2311 .
