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目的 :探讨卡波金川芎嗪联合应用对耳蜗微循环障碍豚鼠的抗氧化作用及部分机制。方法 :50只豚鼠随机分为5组:空白对照组、模型对照组、川芎嗪组、卡波金组、川芎嗪+卡波金组,每组10只。采用光化学法诱导耳蜗微循环障碍模型,并以川芎嗪和/或卡波金进行干预,连续干预1周。采用比色法检测各组豚鼠血清中H_2O_2、MDA、CAT、SOD含量;采用western-blot法检测各组豚鼠耳蜗组织中Nrf-2表达水平。结果 :与空白对照组比较,模型对照组、川芎嗪组、卡波金组、川芎嗪+卡波金组豚鼠血清MDA、H_2O_2含量显著升高,而SOD、CAT活性显著降低(P<0.01);与模型对照组比较,川芎嗪组、卡波金组、川芎嗪+卡波金组豚鼠血清MDA、H_2O_2含量显著降低,而SOD、CAT活性显著升高(P<0.01);与川芎嗪+卡波金组比较,川芎嗪组、卡波金组豚鼠血清MDA和H_2O_2含量显著升高,而SOD、CAT活性显著降低(P<0.01)。与空白对照组比较,其余各组豚鼠耳蜗组织中Nrf-2表达水平均显著升高,有统计学差异(P<0.01);与模型对照组比较,川芎嗪组、卡波金组和川芎嗪+卡波金组豚鼠耳蜗组织中Nrf-2表达水平均显著升高,有统计学差异(P<0.01);与川芎嗪+卡波金组比较,川芎嗪组、卡波金组豚鼠耳蜗组织中Nrf-2表达水平均显著降低,有统计学差异(P<0.01)。结论 :川芎嗪和卡波金联合应用更能提高抗氧化作用,而二者联合应用的抗氧化作用机制可能与上调Nrf-2表达水平相关。
Objective: To investigate the anti-oxidative effect and mechanism of ligustrazine combined with carbopride on guinea pigs with microcirculation disturbance in cochlear. Methods: Fifty guinea pigs were randomly divided into 5 groups: blank control group, model control group, ligustrazine group, carbopol group, ligustrazine + carboptin group, with 10 in each group. The model of cochlear microcirculation was induced by photochemical method, and the rats were interfered by ligustrazine and / or carbopol for 1 week. The contents of H 2 O 2, MDA, CAT and SOD in guinea pigs of each group were detected by colorimetric method. The expression of Nrf-2 in guinea pig cochlea was detected by western-blot. Results: Compared with the blank control group, the contents of MDA and H_2O_2 in the guinea pigs in model control group, ligustrazine group, carbopol group, ligustrazine + carboptin group were significantly increased, while the activities of SOD and CAT were significantly decreased (P <0.01) ; Compared with the model control group, the contents of MDA and H_2O_2 in ligustrazine group, carbopol group, ligustrazine + carboptin group were significantly decreased, while the activities of SOD and CAT were significantly increased (P <0.01) Compared with the Kapok group, the contents of MDA and H_2O_2 in the ligustrazine group and the carbopol group were significantly increased, while the activities of SOD and CAT were significantly decreased (P <0.01). Compared with the blank control group, the expression of Nrf-2 in the cochlear tissues of the other groups were significantly increased (P <0.01). Compared with the model control group, the ligustrazine group, the carbopol group and the ligustrazine group (P <0.01). Compared with Ligustrazine + Carbopol group, Ligustrazine group and Carbopol group had higher levels of Nrf-2 expression in guinea pig cochlea Nrf-2 expression levels were significantly lower, with a statistically significant difference (P <0.01). CONCLUSION: The combination of ligustrazine and carbopol can enhance the anti-oxidant effect. The combined anti-oxidant mechanism may be related to the up-regulation of Nrf-2 expression.