Dexamethasone treatment of murine auditory hair cells and cochlear explants attenuates tumor necrosis factor-α-initiated apoptotic damage
Fig 3
Protective effect of DEX on cell viability, ROS generation, and expression of apoptosis-related proteins in TNF-α-treated cells.
Cells were pretreated with 10 nM DEX for 6 h, followed by treatment with 10 ng/ml TNF-α for a further 24 h. (A) The effect of DEX pretreatment on cell viability reduced by TNF-α. Data in the graph are expressed as means ± SE of four independent experiments. *,# P < 0.05 *; compared with untreated control, #; TNF-α only versus DEX plus TNF-α. (B) Measurement of intracellular ROS accumulation using CM-H2DCFDA. Values are expressed as means ± SE for three independent experiments. *,# P < 0.05 *; compared with untreated control, #; TNF-α only versus DEX plus TNF-α. (C) Representatives immunoblot of apoptosis-related protein expression. Each protein expression was normalized by that of β-actin. The values in a graph are expressed as fold changes relative to the untreated control and expressed as means ± SE of three independent experiments. *,# P < 0.05, ** P < 0.01, *** P < 0.001, *; compared with untreated control, #; TNF-α only versus DEX plus TNF-α.