Fig. 9.
Isoflurane (ISO)-delayed opening of the mitochondrial permeability transition pore (mPTP) was blocked by the disruption of microRNA-21 (miR-21) gene. (A) Representative confocal images of mitochondria. (B) The mPTP opening time. Cardiomyocytes isolated from C57BL/6 wild-type (WT) or miR-21 knockout (KO) mice were treated with Tyrode solution containing 0.5 mM ISO (WT-oxidative stress [OS] +ISO and miR-21 KO-OS+ISO groups) or Tyrode solution without ISO as control (WT-OS and miR-21 KO-OS groups). Tetramethylrhodamine ethyl ester fluorescence image was obtained with a confocal microscope. The mPTP opening was induced by photoexcitation-generated OS and evaluated by measuring the mitochondrial membrane potential. *P < 0.05 versus WT-OS; #P < 0.05 versus WT-OS+ISO (n = 12 cells per group).

Isoflurane (ISO)-delayed opening of the mitochondrial permeability transition pore (mPTP) was blocked by the disruption of microRNA-21 (miR-21) gene. (A) Representative confocal images of mitochondria. (B) The mPTP opening time. Cardiomyocytes isolated from C57BL/6 wild-type (WT) or miR-21 knockout (KO) mice were treated with Tyrode solution containing 0.5 mM ISO (WT-oxidative stress [OS] +ISO and miR-21 KO-OS+ISO groups) or Tyrode solution without ISO as control (WT-OS and miR-21 KO-OS groups). Tetramethylrhodamine ethyl ester fluorescence image was obtained with a confocal microscope. The mPTP opening was induced by photoexcitation-generated OS and evaluated by measuring the mitochondrial membrane potential. *P < 0.05 versus WT-OS; #P < 0.05 versus WT-OS+ISO (n = 12 cells per group).

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