The Expression And Upregulation Mechanism Of Adiponectin And Its Receptors In Hypoxia / Reoxygenation Myocardial

Object: To observe the expression and upregulation mechanism of adiponectin and its receptors in hypoxia / reoxygenation myocardial, and investigate their significance. Methods: Primary cardiomyocytes were obtained from neonatal SD rat and were cultured by enzymatic digestion methods combined with differential attachment method .Cells were identified byα-actin immunofluorescence. Primary cultured 72h cells were used in experiment.①Experimental grouping: Normal control group,Rosiglitazone group, Hypoxia / reoxygenation group, Rosiglitazone + hypoxia / reoxygenation group.②Experimental evaluation: The morphology changes and spontaneous beating case of cardiomyocytes were observed under inverted phase contrast microscope. Adiponectin and adiponectin receptor R1, R2 mRNA expression of myocardial cell were detected using reverse transcription- Polymerase Chain Reaction.Results:①Adiponectin mRNA expression: Rosiglitazone group was significantly higher than the normal control group(P value <0.05). Hypoxia / reoxygenation group was significantly lower than the control group(P value <0.05). Rosiglitazone + hypoxia / reoxygenation group was significantly higher than hypoxia / reoxygenation(P value <0.05).②Adiponectin receptor 1,2 mRNA expression: Rosiglitazone group was significantly higher than the normal control group(P value <0.05). Hypoxia / reoxygenation group was significantly lower than the control group(P value <0.05). Rosiglitazone + hypoxia / reoxygenation group was significantly higher than hypoxia / reoxygenation(P value <0.05).Conclusions: The expression of adiponectin and its receptors were significantly reduced in hypoxia / reoxygenation,but PPARγagonist rosiglitazone can increase the expression in pathological cases. Our results demonstrated that adiponectin and its receptors,involved in myocardial ischemia-reperfusion injury,may be one of the key downstream mechanisms of PPARγagonists in the protective effect against myocardial ischemia-reperfusion injury .