Figure 8
From: Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway
Gentamicin induced mitochondrial dysfunction in cultured cochlear cells. HEI-OC1 cells were treated with gentamicin (20 μM) for different time intervals under hypoxia condition, and (a) mitochondrial membrane potential and (b) the level of ROS production were examined by flow cytometric analysis (n=3). (c) HEI-OC1 cells were incubated with gentamicin (20 μM) for different time intervals under hypoxia condition, and the Bax, Bak, and Bcl-2 expressions were examined by western blot analysis and the quantitative densitometry represented as expressed proteins relative to control group. Results are represented as the mean±s.d. *P<0.05 compared with vehicle group.
