• 主题
高级搜索  >
历史搜索 清空历史
首页> 中文期刊> 《中国病理生理杂志》 >氧化应激激活 JNK-MAPK 参与波动性高血糖诱导的大鼠肝细胞损伤

氧化应激激活 JNK-MAPK 参与波动性高血糖诱导的大鼠肝细胞损伤

         
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

目的：探讨波动性高血糖引起糖尿病大鼠肝细胞凋亡的机制。方法：SD大鼠随机均分为4组：正常对照组、稳定高血糖组、波动高血糖组和胰岛素组。采用链脲佐菌素65 mg／kg 腹腔注射诱发糖尿病，波动高血糖组每天定时腹腔注射速效胰岛素，并错时给予葡萄糖，造成1 d中血糖浓度大幅度波动，12周内波动高血糖组每天血糖波动模式相似，且HbA1c与稳定高血糖组无显著差异。12周后取血和肝脏组织，采用比色法检测超氧化物歧化酶（ SOD）和谷胱甘肽过氧化物酶（ GSH-Px）活性以及丙二醛（ MDA）和一氧化氮（ NO）含量，RT-PCR和West-ern blot检测JNK、p-JNK、Bax和Bcl-2的含量。结果：与正常对照组比较，稳定高血糖组、胰岛素组和波动高血糖组的食物量、饮水量和尿量增加，肝功能异常；MDA含量增多，SOD和GSH-Px活性降低，NO含量减少（P＜0.05）；JNK mRNA、p-JNK蛋白及Bax蛋白水平上调（P ＜0.05），Bcl-2表达减少（P＜0.01）；且波动高血糖组的以上变化均较稳定高血糖和胰岛素组更加明显（ P＜0.05）。结论：波动性高血糖较稳定性高血糖更促进糖尿病肝细胞的凋亡，其机制与JNK-MAPK信号转导通路激活有关。%[ ABSTRACT] AIM:To explore the mechanisms of fluctuant high blood glucose-induced apoptosis of hepatocytes. METHODS:SD rats were randomly divided into normal control group ( N) , stable high blood glucose group ( S) , fluctu-ant high blood glucose group ( F) and insulin group ( I) .Diabetic rats were induced by intraperitoneal injection of strepto-zotocin (65 mg/kg) , and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of ordinary insulin and glucose at different time points every day.The blood glucose fluctuation patterns of the animals in F group with-in 12 weeks were similar every day and no significant difference of the HbA1c concentration was observed compared with S group, indicating that the fluctuant hyperglycemia was successfully established in F group.The activity of superoxide dis-mutase ( SOD) and glutathione peroxidase ( GSH-Px) , and the content of malondialdehyde ( MDA) and nitric oxide ( NO) in the homogenate of the liver tissues were detected by colorimetry.The mRNA and protein levels of JNK, p-JNK, Bax and Bcl-2 were examined by RT-PCR and Western blot.RESULTS:After 12 weeks, the increases in the intakes of food and water, the urine output, and the abnormal liver function were observed in S group, I group and F group.Compared with N group, the MDA level was increased, the content of NO and the activity of SOD and GSH-Px were decreased, and up-regu-lation of JNK mRNA and p-JNK and Bax proteins, and down-regulation of Bcl-2 were also found in S group, I group and F group.The above effects were more obviously showed in F group.CONCLUSION:Oxidative stress activates JNK-MAPK signaling pathway, which is involved in fluctuant high glucose-induced apoptosis of hepatocytes.

著录项

  • 来源
    《中国病理生理杂志》 |2015年第7期|1259-1265|共7页
  • 作者

    李素娟; 金可可; 赵亚萍; 王鹏; 赵文玺; 高凯旋; 杨文娟; 王加林; 吴德平;

  • 作者单位

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    温州医科大学病理生理学教研室;

    浙江温州325035;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

    中国人民解放军第八十二医院内分泌科;

    江苏淮安223001;

  • 原文格式 PDF
  • 正文语种 chi
  • 中图分类 糖尿病;病理生理学;
  • 关键词

    肝细胞; 血糖波动; 氧化应激; JNK-MAPK信号通路;

相似文献

  • 中文文献
  • 外文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号