A mechanism of hair cell damage caused by noise and ototoxic agents is mediated through generation of free radicals and reactive oxygen species(ROS). It is known that most of animals have defense systems of ROS that protect against ROS, and the cochlea of animals also has ROS defense system, which appear efficient in detoxifying ROS generated under normal condition. This system includes several antioxidant enzymes such as superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase (GPX), and glutathione reductase(GR). The radix of Pueraria thunbergiana(P. thunbergiana) is traditionally prescribed to attenuate the clinical manifestation of inner ear dysfunction and various clinical situations including fevers, gastrointestinal disorders, skin problems, migraine headaches, lowering cholesterol, and treating chronic alcoholism in Oriental Medicine. In the present study, to investigate the protection mechanism of ${eta}-sitosterol$ from P. thunbergiana on cisplatin cytotoxicity toward HEI-OC1, we measured the effects of ${eta}-sitosterol$ on activities of SOD, CAT, GPX, and GR in cisplatin treated cells. SOD, CAT, GPX, and GR activities were significantly increased in the presence of 0.001-0.1 ${mu}g/ml$ of ${eta}-sitosterol$ compared to the control group. These results indicate that ${eta}-sitosterol$ protects cisplatin-induced HEI-OC1 cell damage through increasing the antioxidant enzyme system such as SOD, CAT, GPX, and GR.