Role of ginkgo biloba and betahistine dihydrochloride in prevention of gentamicin-induced cochleotoxicity in an experimental model using otoacoustic emission.

In our study the prophylactic role of ginkgo biloba and betahistine dihydrochloride in gentamicin-induced cochleotoxicity is investigated. A total of 30 Wistar albino rat were used in this experiment. Rats were separated into three groups, each with 10 animals, as follows: a- ginkgo biloba group, b- betahistine dihydrochloride group, and c- control group. Before beginning to the experiment, all of the animals were carefully examined otoscopically, making sure that their external ears and tympanic membranes were normal in each animal. For the first step of the experimental protocol, basal cochlear function of each animal was determined by otocoustic emission test. Ip 5 mg/kg betahistine dihydrochloride is performed for 21 days to betahistine group, 10 mg/kg ginkgo biloba to ginkgo biloba group and 0,25 cc salin solution to control group and on the 22nd day, second evaluations of the otoacoustic emission test were performed. The animals in all of the groups were injected with 8 mg/kg gentamicin intraperitoneally for 20 days. The animals continued to receive 5 mg/kg betahistine dihydrochloride in the betahistine group, 10 mg/kg ginkgo biloba in the ginkgo biloba group and salin solution in the control group. During this period of gentamicin administration, obtaining a final otoacoustic emission test at the end of this period. Animals were than sacrificed while still under the effects of high dose xylazine and ketamin. Comparisons within each group and between the groups were achieved based on SNR and DP values obtained in each animal. Statistically, otoacoustic emission values decreased within each group following the gentamicin administration. In the control group, statistical significant decrease on the emission values were determined compared with before and after the gentamicin injection. Thus, ototoxicity became true. Despite the decrease on the emission values of all three groups, after the gentamicin injection, decrease in the groups of ginkgo biloba and betahistine groups is much smaller than the control group, which is statistically non-significant. This result give rise to thought that, agent which are used have prevention properties to gentamicin ototoxicity. Based on DP1000, DP1000, DP2000, SNR1000, SNR 2000, SNR 6000 emission values determination following gentamicin administration, there was a statistically significant difference between the groups. It is seen that, in DP1000, DP1000, DP2000, SNR1000, SNR 6000 emission values ginkgo biloba group, in SNR2000 emission value betahistine group makes this difference. In conclusion, this study suggests that ginkgo biloba and betahistine dihyrdrochloride may have a propyhlactic role in prevention of gentamicin induced ototoxicity. Further studies, particulary with histopathologic verification may be need in the future to support this conclusion.