[Endoplasmic reticulum molecular chaperone involved in the impairment of inner ear consistent with the mimetic aging...

To explore the involvement of endoplasmic reticulum molecular chaperone GRP78 in the impairment of inner ear consistent with the mimetic aging model.

Twenty-four Wistar rats were randomly divided into two groups. Model group was induced by daily hypodermic injection of 10% D-galactose (800 mg x kg(-1) x d(-1)) for 8 weeks and the control group was given saline accordingly. Spatial learning and memory was measured by Morris-Water-Maze. Colorimetry was used to analyze superoxide dismutase (SOD) and malondialdehyde (MDA) extracted from inner ear tissue. Hearing threshold of rats were detected with Auditory brainstem response (ABR). In addition, expression of GRP78 in the inner ear was detected by immunohistochemistry, RT-PCR and Western blot. The control group was studied parallel.

The escape latency in the model group injected with D-galactose was markedly longer than that in the control group. Accordingly, the changes of SOD and MDA were more significant in the model group, the difference between two groups was significant (t-test, P<0.01). the variation of ABR in two groups was observed, There was no statistically difference of the hearing in the model group compared with the control group (P>0.05). The expression of GRP78 was significantly different between two groups, which is increased in the inner ear tissue of model group (P<0.01).

The impairment of inner ear tissue partly dued to the oxidative stress in the model, which was induced by D-galactose and endoplasmic reticulum molecular chaperone was thought to contribute to the impairment mechanism of inner ear in mimetic aging model.