水杨酸诱导大鼠耳鸣模型下丘脑神经细胞氧化损伤及凋亡调节蛋白Bcl-2与Bax的表达

【目的】探讨水杨酸诱导耳鸣与氧自由基代谢、脂质过氧化，以及神经细胞凋亡的关系。【方法】运用生化法测定水杨酸诱导耳呜大鼠下丘脑神经细胞组织中超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量的变化，运用脱氧核糖核苷酸末端转移酶介导的缺口末端标记技术（TUNEL）和WesternBlot（WB）法检测神经细胞凋亡调节蛋白Bcl一2与Bax。【结果】水杨酸组SOD活性明显下降，MDA含量明显增高，同时神经细胞凋亡增加，bax／bcl一2比值降低。【结论】下丘脑氧自由基代谢紊乱、脂质过氧化损伤及神经细胞凋亡与水杨酸诱发耳呜的发生发展有关。

Oxidative Injury and the Expression of Apoptotic Proteins Bcl-2 and Bax in Nerve Cells of Hy- pothalamus in Rat Tinnitus Induced by Salicylic Acid

[Objective]To explore the tinnitus induced by salicylic acid and its relationship with oxygen radical metabolism, lipid peroxidation and nerve cell apoptosis. [Methods] Biochemistry method was used to measure the activity of superoxide dismutase（SOD） and the concentration of malondialdehyde（MDA） in nerve cells of hypothalamus in rat tinnitus induced by salicylic acid. TUNEL and Western Blot were used to detect the expression of apoptotic proteins Bcl-2 and Bax in nerve cells. [Results]In salicylic acid group, the activity of SOD decreased obviously and MDA level increased markedly, meanwhile nerve cell apoptosis elevated and Bax/Bcl-2 ratio reduced. [Conclusion] Oxygen radical metabolic disorder, lipid peroxide injury and neuron ap- optosis in hypothalamus are associated with the occurrence and development of tinnitus induced by salicylic acid.