Background: Age-related hearing impairment is one of the most common complaints among older people. It was reported that central neural processing deficits contribute this deficit and improving central auditory function might be beneficial for cognitive functions in elderly. In the present study, we examined the effect of rosmarinic acid (RA) on auditory evoked oscillations and lipid peroxidation in D-galactose induced rat aging model. Methods: Wistar rats were randomly divided into four groups: sham (S); RA-treated (R); D-galactose-treated (DG); D-galactose + RA-treated (DGR). After eight weeks period, central auditory functions were evaluated by measuring the auditory evoked oscillations over temporal cortex. Thiobarbituric acid reactive substances (TBARS) assay was used to quantify lipid peroxidation levels of the temporal cortex. Results: D-galactose treated rats exhibited attenuated auditory evoked delta, alpha and beta responses. Moreover, increased lipid peroxidation levels were detected in the D-galactose treated rats. Eight weeks RA (50 mg/kg) treatment significantly improved oscillatory alterations and lipid peroxidation as compared to DG group. Conclusion: Thus, present study shows D-galactose induced oscillatory changes in auditory processing and highlights the protective effect of RA against D-galactose induced changes in auditory evoked oscillations and lipid peroxidation.
Decrease of Auditory Evoked Delta, Alpha and Beta Oscillatory Responses in D-galactose Induced Aging Model: Effects of Rosmarinic Acid
Hidisoglu E.;
2018-01-01
Abstract
Background: Age-related hearing impairment is one of the most common complaints among older people. It was reported that central neural processing deficits contribute this deficit and improving central auditory function might be beneficial for cognitive functions in elderly. In the present study, we examined the effect of rosmarinic acid (RA) on auditory evoked oscillations and lipid peroxidation in D-galactose induced rat aging model. Methods: Wistar rats were randomly divided into four groups: sham (S); RA-treated (R); D-galactose-treated (DG); D-galactose + RA-treated (DGR). After eight weeks period, central auditory functions were evaluated by measuring the auditory evoked oscillations over temporal cortex. Thiobarbituric acid reactive substances (TBARS) assay was used to quantify lipid peroxidation levels of the temporal cortex. Results: D-galactose treated rats exhibited attenuated auditory evoked delta, alpha and beta responses. Moreover, increased lipid peroxidation levels were detected in the D-galactose treated rats. Eight weeks RA (50 mg/kg) treatment significantly improved oscillatory alterations and lipid peroxidation as compared to DG group. Conclusion: Thus, present study shows D-galactose induced oscillatory changes in auditory processing and highlights the protective effect of RA against D-galactose induced changes in auditory evoked oscillations and lipid peroxidation.
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