Effects of adipose stem cells on miR-423-5p and PI3K/AKT pathways in myocardial tissue of rats with myo-cardial infarction
Objective To investigate the effects of adipose mesenchymal stem cells on miR-423-5p,PI3K,and AKT in myocardial tissue of myocardial infarction model rats.Methods The rats were randomly divided into 3 group:control group,MI model group(MI),MI+adipose-derived stem cells(MI+rADSCs)intervention group,with 6 rats in each group.After anesthesia,the rats in control group were opening the chest and suture,the rats in MI model group and MI+rADSCs group was ligatured anterior descending branch.106 adipose stem cells(adscs)were injected in rats'heart of the MI+rADSCs group before suture.Heart's weight was measured,and the pathological changes were observed by HE staining and Masson staining.Real-time quantitative PCR was used to detect the mRNA expression of miR-423-5p,PI3K and Akt.Western blot was used to detect the protein expression of Akt,p-AKT,PI3K and p-PI3K.Results Compared with the control group,the cardiac tissue mass of the MI model group and the MI+rADSCs group was significantly increased,and the difference between the MI group and the control group was statistically significant(P＜0.05).The pathological results showed that the arrangement of myocardial cells was disordered,the degeneration and necrosis of myocardial cells were serious,the collagen fibers were precipitat-ed,and obvious inflammatory infiltration was found in the myocardial cells of the MI group.Compared with the MI group,the myocardial necrosis,inflammatory infiltration and collagen deposition in the MI+rADSCs group were sig-nificantly lower than those.Compared with the control group,the mRNA expression levels of PI3K,AKT,Mir-423-5p and the protein expression levels of p-PI3K,p-AKT in myocardial tissue of the MI group were significantly higher(P＜0.05).The expression level of the above indexes in the MI+rADSCs group was significantly lower than that in the MI group(P＜0.05).Conclusion Adipose-derived stem cells can reduce myocardial injury and fibrosis,and im-prove cardiac function after myocardial infarction.The mechanism may be that miR-423-5p can inhibit the transcrip-tion and protein phosphorylation of PI3K and Akt,and protect and treat myocardial infarction.
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