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目的 通过观察川芎嗪对顺铂诱导豚鼠耳蜗毛细胞中JNK、c-JUN及Caspase-3蛋白表达水平的影响,探讨其抗凋亡的机制.方法 将60只听力正常的健康白毛红目豚鼠按照随机字数表法分为空白组与模型组,空白组豚鼠正常饲养,模型组豚鼠腹腔注射顺铂,诱导药物性耳聋模型.造模成功后,将空白组及模型组分别随机分为两组,即空白对照组、空白+川芎嗪组、模型对照组、模型+川芎嗪组.空白+川芎嗪组、模型+川芎嗪组豚鼠腹腔注射川芎嗪注射液进行干预,2周后处死豚鼠,采用Western-blot法对各组豚鼠耳蜗组织中c-JUN、JNK及Caspase-3蛋白表达水平进行检测.结果 与空白组相比,模型组豚鼠听性脑干反应(ABR)阈值显著提高,差异有统计学意义(P＜0.01);空白组豚鼠耳蜗毛细胞排列整齐、均匀,无缺失及坏死细胞出现;模型组豚鼠耳蜗毛细胞变形明显,排列不均,溶解破坏的毛细胞较多.与空白对照组和空白+川芎嗪组比较,模型对照组豚鼠耳蜗组织中c-JUN、JNK、Caspase-3蛋白表达水平均显著升高,差异有统计学意义(P＜0.01).与模型对照组比较,模型+川芎嗪组豚鼠耳蜗组织中c-JUN、JNK、Caspase-3蛋白表达水平降低,差异有统计学意义(P＜0.05).结论 川芎嗪可通过调控JNK/c-JUN信号通路的活化,进而调控Caspase-3来抑制细胞凋亡途径,进而发挥其抗凋亡作用.“,”Objective By observing the index of JNK,c-JUN and Caspase-3 protein of cisplatin induced hearing loss guinea pigs to investigate the internal channel how ligustrazine inhibit the apoptosis of cochlear hair cells.Methods A total of 60 healthy and normal hearing guinea pigs were randomly divided into the blank group and model group.The guinea pigs of the blank group were normally fed,and the guinea pigs of the model group were injected intraperitoneally cisplatin to make deafness model.After the model replication was successful,the guinea pigs of blank group and model group were randomly divided into 2 groups,a total of 4 groups:blank control group,blank + ligustrazine group,model control group,model + ligustrazine group.The guinea pigs of the blank + ligustrazine group and the model + ligustrazine group were injected intraperitoneally ligustrazine injection to interve.After 2 weeks,the guinea pigs were killed,adopting the detection of Western-blot to observe the expression of c-JUN,JNK and Caspase-3 proteins in the cochlea tissues of guinea pigs.Results Compared with the blank group,the ABR threshold of the guinea pigs in the model group was significantly improved (P ＜ 0.01);the blank group of guinea pig cochlear hair cells arranged in neat and uniform,there was no deletion and cell necrosis;in the model group,deformation of guinea pig cochlear hair cells were obviously,arranged unevenly,dissolved damaged more.The expression levels of c-JUN,JNK and Caspase-3 in cochlear tissues of guinea pigs of the model control group increased significantly compared with the blank control group and the blank + ligustrazine group(P ＜ 0.01).Compared with the model control group,the expression levels of c-JUN,JNK and Caspase-3 in cochlear tissues of guinea pigs in the model + ligustrazine group reduced (P ＜ 0.05).Conclusion Ligustrazine can activate the signaling pathway of JNK/c-JUN,and then inhibit the channel of apoptosis by controlling Caspase-3 to exert its anti apoptotic effect.