糖尿病大鼠胃黏膜细胞色素C异常表达及大黄素调控
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  • 英文篇名:Effect of emodin on expression of cytochrome c in gastric mucosa of diabetic rats
  • 作者:徐富翠 ; 赵宏贤 ; 杨晓红 ; 郭勇
  • 英文作者:Xu Fucui;Zhao Hongxian;Yang Xiaohong;Guo Yong;Department of Histology and Embryology of Luzhou Medical College;
  • 关键词:糖尿病 ; 胃黏膜 ; 细胞色素C ; 细胞凋亡 ; 大黄素
  • 英文关键词:Diabetes;;Gastric mucosa;;Cytochrome C;;Cell death
  • 中文刊名:LXYB
  • 英文刊名:Journal of Luzhou Medical College
  • 机构:泸州医学院基础医学院组胚教研室;
  • 出版日期:2014-02-20
  • 出版单位:泸州医学院学报
  • 年:2014
  • 期:v.37
  • 基金:四川省卫生厅资助项目(100242);; 泸州市科技局重点项目(2009-S-15(5/7)
  • 语种:中文;
  • 页:LXYB201401022
  • 页数:4
  • CN:01
  • ISSN:51-1264/R
  • 分类号:87-90
摘要
目的:探讨糖尿病胃病的相关机制及大黄素干预。方法:SD大鼠随机分为对照组(正常组)、实验组(糖尿病组)与大黄素组,实验组应用腹腔一次性注射链脲佐菌素(streptozotocin,STZ)建立糖尿病大鼠模型,造模成功10周后免疫组织化学检测胃黏膜腺细胞细胞色素C(cytc)的表达情况。结果:①实验组和大黄素组大鼠于造模后均出现多尿、多饮、多食症状,体重减轻,平均体重明显低下对照组(P<0.05);平均血糖浓度显著高于对照组(P<0.05)等糖尿病症状。但应用大黄素干预组大鼠的血糖浓度显著低于实验组。②实验组cyt c蛋白阳性表达的胃黏膜细胞数明显高于对照组(P<0.05;大黄素组cyt c蛋白阳性表达的胃黏膜细胞数明显少于实验组(P<0.05)。结论:糖尿病引起大鼠胃黏膜细胞高表达cyt c蛋白,导致细胞死亡增加,参与糖尿病胃病的发生,而大黄素可降低胃黏膜细胞cyt c蛋白表达,从而缓解糖尿病胃病。
        Objective:To investigate the pathegenetic mechanism and effect of emodin on gastric disturbance of diabetic rats.Methods:SD rats were randomly divided into control group,diabetic group and emodin group.Ten weeks later,expression of cytochrome C in gastric mucosa was detected by immunohistochemistry.Results:(Din diabetic group and emodin group,typical symptoms of diabetes appeared,the average weight was significantly lower(P< 0.05),and the blood glucose was significantly higher than those in control group(P< 0.05).(2) Compared with rats in control group,the cytochrome C in diabetic group was significantly higher {P < 0.05).Compared with diabetic group,the cytochrome C in emodin group was significantly lower(P < 0.05).Conclusion:Diabetes causes high expression of cytochrome C in gastric mucosal cells,which induces cell death and gastric disturbance of diabetic rats.Emodin may decrease cytochrome C in gastric mucosa and therefore,alleviate the gastric disturbance of betic rats.
引文
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