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作 者:白雪思 高军[1] 马贤德[2] BAI Xuesi;GAO Jun;MA Xiande(Shengjing Hospital of China Medical University,Shenyang 110004,Liaoning,China;Liaoning University of Traditional Chinese Medicine,Shenyang 110847,Liaoning,China)
机构地区:[1]中国医科大学附属盛京医院耳鼻咽喉科,辽宁沈阳110004 [2]辽宁中医药大学,辽宁沈阳110847
出 处:《中华中医药学刊》2018年第9期2261-2264,I0016,共5页Chinese Archives of Traditional Chinese Medicine
基 金:辽宁省科技厅项目(2013020190)
摘 要:目的:通过观察川芎嗪和/或卡波金对耳蜗微循环障碍豚鼠耳蜗组织Nrf2/ARE信号通路的调控作用,探讨川芎嗪联合卡波金的抗氧化作用机制。方法:豚鼠50只,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。分别给予川芎嗪和/或卡波金干预,每日一次,连续7 d。末次干预后1 h,取耳蜗组织,采用免疫组织化学法检测耳蜗组织中Keap1表达水平,采用western-blot法检测p-Nrf2、NQO1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+卡波金组豚鼠耳蜗组织中Keap1、p-Nrf2、NQO1的表达水平显著升高(P〈0.01);与模型对照组比较,川芎嗪组、卡波金组、川芎嗪+卡波金组豚鼠耳蜗组织中Keap1表达水平显著降低,p-Nrf2、NQO1的表达水平显著升高(P〈0.01);与川芎嗪+卡波金组比较,川芎嗪组、卡波金组豚鼠耳蜗组织中Keap1表达水平显著升高,p-Nrf2、NQO1的表达水平显著降低(P〈0.01)。结论:川芎嗪联合卡波金对耳蜗微循环障碍豚鼠的抗氧化作用可能是通过调控Nrf2/ARE通路实现的。Objective: through the observation of ligustrazine and/or cabo gold on cochlear microcirculation guinea pig cochlear organization Nrf2/motorcycle regulatory role of signaling pathways,ligustrazine combine cabo antioxidation mechanism of gold. Methods: 50 guinea pigs were randomly divided into 5 groups: blank control group; Model control group; Ligustrazine group; Capojin group; Ligustrazine + capojin group,10 in each group. The microcirculation obstacle model of cochlea was induced by photochemical method. The intervention of ligustrazine and/or carbopin was administered once a day for 7 days. 1 hour after the last intervention,cochlear tissue was taken and immunohistochemical method was used to detect the expression level of Keap1 in cochlea,and the expression level of p-nrf2 and NQO1 was detected by western-blot method. Results: compared with blank control group,model control group,ligustrazine group,cabo gold group,ligustrazine + cabo gold guinea pig cochlear tissues Keap1,p-Nrf2,significantly increased the expression level of NQO1( P〈 0. 01); Compared with the control group,the expression level of Keap1 in the cochlea group of guinea pig cochlea was significantly decreased,and the expression level of p-nrf2 and NQO1 was significantly increased( P〈 0. 01). The expression level of Keap1 was significantly increased in the cochlea group of guinea pig cochlea with ligustrazine and kapojin group,and the expression level of p-nrf2 and NQO1 was significantly decreased( P〈 0. 01).Conclusion: the antioxidation effect of ligustrazine combined with carbopin on microcirculation of cochlea in guinea pigs may be achieved by regulating the Nrf2/ARE pathway.
关 键 词:卡波金 川芎嗪 耳蜗微循环障碍 氧化应激 Nrf2/ARE通路
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