Objective: To investigate the protective mechanism of zinc finger protein A20 over-expression in acute myocardial infarction (AMI) rats.
Methods: Forty-five Sprague Dawley (SD) rats were randomly divided into sham group, model group and observation group. The model and observation groups were injected with normal saline and pcDNA3.1-A20 plasmid in the pre-operative 24 hour, respectively. The AMI model was established by ligating the left anterior descending coronary arteries of the model group and the observation group. The sham group were only treated with left anterior descending coronary artery threading but not ligation. The levels of A20 messenger ribonucleic acids (mRNA) and protein were detected by, reverse transcription polymerase chain reaction (RTPCR) and Western blot. The levels of tumour necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) proteins in the peripheral blood were detected by the enzyme-linked immunosorbent assay (ELISA). The myocardial infarct size was analysed by triphenyl tetrazolium (TTC) staining.
Results: Compared with the sham group, the levels of A20 mRNA and protein in the myocardium of the model and observation groups were significantly increased; the level in observation group was significantly higher than that of model group (p < 0.05). Compared with sham group, the level of nuclear factor-κB (NF-κB) p65 protein in the myocardium of the model and observation groups was activated into the nucleus, and NF-κB p65 protein in the nucleus in the observation group was significantly lower than that of the model group (p < 0.05). Compared with the sham group, the levels of TNF-α and IL-6 proteins in the peripheral blood in the model and observation groups were significantly increased (p < 0.05). The myocardial infarct size was significantly increased in the model and observation groups (p < 0.05), while the myocardial infarct size in the observation group was significantly decreased compared with the model group (p < 0.05).
Conclusion: Zinc finger protein A20 can significantly inhibit the inflammatory injury and cell apoptosis process in AMI rats, which may be related to its inhibition of the expression and activation of nuclear transcription factor NF-κB.