Mechanism of gentamicin induced ototoxicity and the neuroprotective effect mediated by baicalin

De DAI

ABSTRACT

BACKGROUND:

Gentamicin(GM) -induced ototoxicity relates to the permanent injury on the spinal ganglion cells, which are important to the process of hearing and communication.

OBJECTIVE:

To investigate the mechanism underlying antioxidant effect of baicalin(BA) on GM-treated mouse spinal ganglion cells (SCGs).

DESIGN:

Randomized controlled trial.SETTING and MATERIALS The research was completed in the Guandong Medical College. Twenty Kunming mice of either gender( clean grade) weighing(15±2) g were provided by the Experimental Animal Center of Guangdong Medical College (certificate number 2003A026). The mice were kept at the environment temperature of 28℃ with relative humidity of 70%.

INTERVENTIONS:

Twenty mice were randomly divided into control group , GM group(with GM treatment only), BA group(with BA treatment only)and GM + BA group(with GM combined with BA treatment). GM was administered in the GM and GM + BA groups via intraperitoneal injection at 100 mg/kg for 10 consecutive days, and BA was given in BA and GM + BA groups similarly at 100 mg/kg. In the control group, the mice Received saline injection in equivalent volume in the same manner.MAIN OUTCOME

MEASURES:

The activities of the antioxidative enzymes superoxide dismutase(T-SOD) and glutathione peroxidase(GSH-PX) were evaluated and the contents of lipid peroxidation substance malondialdehyde (MDA) measured with ultraviolet (UV) chromatography in SCGs in different treatments.

RESULTS:

BA could reverse the GM-induced low activities of T-SOD (from 46. 50 to 27.86 NU/mL, P ＜ 0. 01) and GSH-PX(from 83.77 to 42. 34 U,P ＜ 0. 01 ) , and limited the GM-induced high content of MDA(from 11.87 to 17.03 μmol/L, P ＜ 0.01) in SGC.

CONCLUSION:

BA produces neuroprotective effect on SGCs through eliminating superoxide radicals and inhibiting lipid peroxidation in the event of GM exposure.