LncRNA-TUG1 Mediated Cardiac Function Injury After Myocardial Infarction In Mice By Affecting ENOS And BDNF

Objective: To investigate the expression changes of long non-coding RNA-taurine up-regulated gene 1(lnc RNA-TUG1)after myocardial infarction,and the role of lnc RNA-TUG1 in myocardial injury after myocardial infarction(MI)by influencing endothelial nitric oxide synthase(e NOS)and brain-derived neurotrophic factor(BDNF).Methods: Forty healthy male C57BL/6 mice were randomly divided into sham group,myocardial infarction group(MI group),myocardial infarction +empty carrier group(MI+sh NC group),myocardial infarction + lnc RNA-TUG1 silencing group(MI+sh TUG1 group),with 10 mice in each group.lnc RNA-TUG1 silenced adenovirus or empty vector adenovirus was constructed and injected into the tail vein to infect mice in the corresponding group.One week after infection,myocardial infarction model was established by ligation of the left anterior descending branch of coronary artery.The sham group performed the same operations except no ligation.One week after the model was constructed,the changes in cardiac function of mice were detected by small animal ultrasound apparatus.After the examination,orbital blood was taken and cardiac tissue was collected for follow-up examination.The expression of lnc RNA-TUG1 in myocardial infarction area was detected by RT-q PCR,the level of markers of cardiac injury in plasma was assessed by ELISA,the difference of myocardial infarction area was compared by TTC staining,and the changes of myocardial e NOS and BDNF in myocardial infarction area were detected by Western blot.The levels of inflammation and mitochondrial biosynthesis related proteins were evaluated by Western blot,ELISA and RT-q PCR.Results: 1.The expression of lnc RNA-TUG1 in myocardial of mice in MI group was significantly up-regulated compared with that in sham group,and the expression of lnc RNA-TUG1 in MI+sh TUG1 group was significantly reduced compared with that in MI+sh NC group;2.Compared with the sham group,the expression of myocardial injury markers in MI group was significantly increased,and the expression of myocardial injury markers in MI+sh TUG1 group was significantly decreased compared with that in MI+sh NC group;3.The ultrasonic cardiac results of small animals showed that the cardiac function of mice in MI group was significantly decreased compared with that in sham group,and the cardiac function of mice in MI+sh TUG1 group was significantly improved compared with that in MI+sh NC group;4.TTC staining results showed that the white infarct area in the heart sections of mice in MI group was significantly increased compared with that in sham group,and the white infarct area in MI+sh TUG1 group was significantly decreased compared with that in MI+sh NC group;5.Compared with sham group,the expression of inflammatory cytokines and the release of related messenger RNA(m RNA)in myocardial tissue of mice in MI group were significantly increased,and the expression of inflammatory cytokines and m RNA in MI+sh TUG1 group was significantly decreased after silenting the expression of lnc RNA-TUG1;6.Compared with mice in the sham group,the expressions of mitochondrial biosynthesis-related proteins and m RNA corresponding to proteins in the MI group were significantly reduced,and the release and expression of mitochondrial biosynthesis-related proteins in the MI+sh TUG1 group were significantly improved compared with those in the MI+sh NC group;7.Compared with sham group,the expressions of e NOS and BDNF in myocardial tissue of mice in MI group were significantly decreased,and those in MI+sh TUG1 group were significantly increased compared with MI+sh NC group.Conclusion: Myocardial infarction can increase the expression of lnc RNA-TUG1 in mouse myocardium.Inhibition of lnc RNA-TUG1 can improve the cardiac function injury and the spread of infarction size in mice after myocardial infarction by affecting the inflammatory response and mitochondrial biosynthesis mediated by e NOS and BDNF in mouse myocardial tissue.