水杨酸钠引起动物耳鸣是目前最常用的耳鸣动物模型，但研究显示，对水杨酸钠耳鸣动物治疗有效的药物对人类耳鸣无效，这提示水杨酸钠耳鸣动物模型并不完全适合研究人类耳鸣。可能的原因是水杨酸钠耳鸣动物模型与临床上水杨酸钠引起的耳鸣机制不同。临床上水杨酸钠用于机体出现炎症后的抗炎药，此时体内的环加氧酶-1（cyclooxygenase-1，COX-1）和环加氧酶-2（COX-2）均被激活，水杨酸钠通过抑制COX-1和COX-2发挥抗炎作用，并引起耳鸣。而水杨酸钠耳鸣动物模型中，均是在正常动物中诱导耳鸣，此时体内只有COX-1激活，COX-2没有激活，水杨酸钠通过抑制COX-1引起动物耳鸣。为了更好地研究COX抑制剂引起耳鸣的机制，本研究通过分别敲除COX-1 基因和COX-2基因的小鼠，在正常及炎症条件下应用COX抑制剂，探讨COX-1和COX-2在耳鸣机制中的作用，为临床上耳鸣的治疗提供理论依据。

Sodium salicylate animal tinnitus is by far the most common tinnitus animal model, but research shows that effective drug treatment of sodium salicylate tinnitus animals is invalid in humans, suggesting sodium salicylate tinnitus animal model is not suitable for human. Possible reason is that the mechanisms of sodium salicylate tinnitus animal models and clinical sodium salicylate tinnitus are different. Sodium salicylate is clinically used in the body after inflammation, while both cyclooxygenase - 1 (COX- 1) and cyclooxygenase – 2 (cox-2) are activated, playing the role of anti-inflammatory through inhibiting COX – 1 and cox-2 and causing tinnitus. But sodium salicylate tinnitus animal models are induced in normal condition, which can only activate COX – 1without cox-2 being activated, thus sodium salicylate tinnitus is caused by inhibition of COX - 1.In order to better study the mechanism of COX inhibitor causing tinnitus, we knockout COX - 1 and cox-2 gene respectively in mice in this study, applying COX inhibitors under the conditions of normal and inflammation, probing into the role of COX - 1 and cox-2 in tinnitus mechanism, as to providing theoretical basis for clinical treatment of tinnitus.