Liang Bing,Fang Jie.Protective effect of isoflurane on H9c2 cells from hypoxia-reoxygenation injury via Nrf2-ARE signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(14):1615-1621.
Liang Bing,Fang Jie.Protective effect of isoflurane on H9c2 cells from hypoxia-reoxygenation injury via Nrf2-ARE signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(14):1615-1621.DOI:
Protective effect of isoflurane on H9c2 cells from hypoxia-reoxygenation injury via Nrf2-ARE signaling pathway
Objective To investigate the protective effect of isoflurane on H9c2 cell injury induced by hypoxia-reoxygenation via Nrf2-ARE signaling pathway. Methods H9c2 cells were cultured and divided into control group
hypoxia-reoxygenation group
isoflurane pre-treatment group
Nrf2 siRNA transfection group
nonspecific transfection group (scramble group)
nonspecific transfection with isoflurane pretreatment group
and Nrf2 siRNA transfection with isoflurane pretreatment group. Cell viability and apoptosis were evaluated by MTT assay and TUNEL assay
respectively. The levels of MDA and GSH were tested with TBA method and spectrophotometric method. qRT-PCR and Western blotting were performed to detect the expression of Nrf2
HO-1 and NQO1 at mRNA and protein levels. Results Compared with the control group
the decreased cell viability
increased cell apoptosis
raised MDA level
and descended GSH level were observed in the hypoxia-reoxygenation group. Meanwhile
both of the mRNA and protein levels of Nrf2
HO-1 and NQO1 were remarkably down-regulated in the hypoxia-reoxygenation group compared with the control group (P0.05). Isoflurane pre-treatment significantly improved H9c2 cell viability
reduced the number of apoptotic cells
decreased MDA level and increased GSH level compared with the hypoxia-reoxygenation group (P0.05). Furthermore
the mRNA and protein levels of Nrf2
HO-1 and NQO1 in H9c2 cells were also up-regulated after isoflurane treatment (P0.05). Compared with the hypoxia-reoxygenation group and the scramble group
the expression of Nrf2 in the siRNA transfection group was significantly decreased (P0.05)
and 2% isoflurane had no significant effect on the expression of Nrf2. The cell viability was significantly decreased
and apoptotic cells were notably increased in the Nrf2 siRNA transfection with isoflurane pretreatment group compared with the control group
isoflurane pretreatment group and nonspecific transfection with isoflurane pretreatment group (P0.05). Meanwhile
the MDA level was notably up-regulated
and the GSH level was remarkably down-regulated in the Nrf2 siRNA transfection with isoflurane pretreatment group. Conclusion The protective effect of isoflurane on hypoxia-reoxygenation-injured H9c2 cells is confirmed
and it is possibly related with the activation of Nrf2-ARE signaling pathway.