Fig. 1.
MicroRNAs play an important role in isoflurane-mediated protection of cardiomyocytes. (A) Isoflurane exposure causes changes in expression levels of microRNAs. MicroRNA expression changes were measured by quantitative real-time polymerase chain reaction in the in vitro neonatal rat cardiomyocyte model (black bars) and in the in vivo rat model (white bars) after exposure to 30 min of isoflurane followed by a 15-min washout period. n = 6; all data = P < 0.05 compared with control without isoflurane exposure. (B) miR-21 is transiently up-regulated by isoflurane in cardiomyocytes. miR-21 increased significantly after a 30-min exposure to isoflurane, followed by a 15-min washout period. miR-21 expression was measured 3, 6, and 24 h after exposure. Expression decreased over time and returned to baseline after 3 h. n = 6, *P < 0.05 compared with non–isoflurane-exposed control. (C) Anti-miR-21 transfection dose-dependently knocks down the expression of miR-21. Neonatal rat cardiomyocytes were treated with 1, 5, and 25 nM of transfection reagent for 20 h. miR-21 expression was decreased in a dose-dependent manner and significantly knocked down in the 25 nM transfection group. n = 6, *P < 0.05 compared with control. (D) Anti-miR-21 transfection knocks down the expression of miR-21 after isoflurane exposure. Cultured neonatal rat cardiomyocytes were treated with media, 25 nM of microRNA scramble inhibitor, or 25 nM of anti-miR-21 for 20 h. miR-21 expression was increased in nontreated and scramble-transfected groups after isoflurane exposure. miR-21 expression was significantly knocked down in both control and isoflurane-exposed groups. n = 6, *P < 0.05 compared with nontreated and scramble-transfected controls. #P < 0.05 compared with non–isoflurane-exposed controls. (E) Anti-miR-21 abolishes the protective preconditioning effect of isoflurane. miR-21–transfected cells showed no significant difference in lactate dehydrogenase (LDH) release between isoflurane and control groups. Cells were exposed to 50 μM of hydrogen peroxide for 6 h. Nontreated and scramble-transfected controls showed significantly decreased LDH release when exposed to 30 min of isoflurane before hydrogen peroxide exposure. n = 6, *P < 0.05 compared with controls.

MicroRNAs play an important role in isoflurane-mediated protection of cardiomyocytes. (A) Isoflurane exposure causes changes in expression levels of microRNAs. MicroRNA expression changes were measured by quantitative real-time polymerase chain reaction in the in vitro neonatal rat cardiomyocyte model (black bars) and in the in vivo rat model (white bars) after exposure to 30 min of isoflurane followed by a 15-min washout period. n = 6; all data = P < 0.05 compared with control without isoflurane exposure. (B) miR-21 is transiently up-regulated by isoflurane in cardiomyocytes. miR-21 increased significantly after a 30-min exposure to isoflurane, followed by a 15-min washout period. miR-21 expression was measured 3, 6, and 24 h after exposure. Expression decreased over time and returned to baseline after 3 h. n = 6, *P < 0.05 compared with non–isoflurane-exposed control. (C) Anti-miR-21 transfection dose-dependently knocks down the expression of miR-21. Neonatal rat cardiomyocytes were treated with 1, 5, and 25 nM of transfection reagent for 20 h. miR-21 expression was decreased in a dose-dependent manner and significantly knocked down in the 25 nM transfection group. n = 6, *P < 0.05 compared with control. (D) Anti-miR-21 transfection knocks down the expression of miR-21 after isoflurane exposure. Cultured neonatal rat cardiomyocytes were treated with media, 25 nM of microRNA scramble inhibitor, or 25 nM of anti-miR-21 for 20 h. miR-21 expression was increased in nontreated and scramble-transfected groups after isoflurane exposure. miR-21 expression was significantly knocked down in both control and isoflurane-exposed groups. n = 6, *P < 0.05 compared with nontreated and scramble-transfected controls. #P < 0.05 compared with non–isoflurane-exposed controls. (E) Anti-miR-21 abolishes the protective preconditioning effect of isoflurane. miR-21–transfected cells showed no significant difference in lactate dehydrogenase (LDH) release between isoflurane and control groups. Cells were exposed to 50 μM of hydrogen peroxide for 6 h. Nontreated and scramble-transfected controls showed significantly decreased LDH release when exposed to 30 min of isoflurane before hydrogen peroxide exposure. n = 6, *P < 0.05 compared with controls.

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