Effects of plasma exosome⁃derived miR⁃29b⁃3p on myocardial cell inj ury in hypoxia/reoxygenation after sevoflurane postconditioning via targeting IGF1 / 安徽医科大学学报
Acta Universitatis Medicinalis Anhui
; (6): 1450-1457, 2023.
Article
de Zh
| WPRIM
| ID: wpr-1038468
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WPRO
ABSTRACT
Objective @#The purpose of this study was to investigate the effects of plasma exosome⁃derived miR⁃29b⁃3p in myocardial ischemia⁃reperfusion injury ( MIRI) rats on hypoxia/reoxygenation ( H/R) cardiomyocyte after sevoflurane (SEV) postconditioning through targeting IGF1 . @*Methods @# The GEO database was used to screen differentially expressed miRNAs in MIRI , and cardiomyocytes were treated with H/R to construct a MIRI cell model. The expression of miR⁃29b⁃3p and IGF1 in the MIRI cell model post⁃treated with SEV was intervened , and then the survival rate of cardiomyocytes was detected by MTT , apoptosis was detected by flow cytometry , and inflammatory factors (IL⁃1β and TNF⁃α ) in cardiomyocytes in each group were detected by ELISA.@*Results @#Compared with Normal group , the expression of miR⁃29b⁃3p in plasma exosomes of MIRI rats was enhanced (P < 0. 05) , and the target⁃binding relationship between miR⁃29b⁃3p and IGF1 was confirmed ( P < 0. 05) . After SEV post⁃treatment , the expression of miR⁃29b⁃3p in H/R⁃stimulated cardiomyocytes decreased , while the expression of IGF1 increased (both P < 0. 05) . Overexpression of miR⁃29b⁃3p in plasma exosomes could significantly inhibit the survival rate of H/R cells after SEV treatment , aggravate apoptosis and inflammatory response , while knockdown of miR⁃29b⁃3p showed a opposite effects (all P < 0. 05) . The rescue experimental data showed that overexpression of IGF1 could partially reverse the effects of overexpression of miR⁃29b⁃3p on H/R cell injury after SEV treatment ( all P <0. 05) .@*Conclusion @#Plasma exosome⁃derived miR⁃29b⁃3p promotes H/R cardiomyocyte injury after SEV treatment by targeting IGF1 .
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WPRIM
langue:
Zh
Texte intégral:
Acta Universitatis Medicinalis Anhui
Année:
2023
Type:
Article