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灯盏花素对糖尿病大鼠肝脏保护作用的实验研究
引用本文:夏玲玲,魏伟,林辉,周典,钱浩,赵岷,吴永贵.灯盏花素对糖尿病大鼠肝脏保护作用的实验研究[J].中国药理学通报,2004,20(6):664-668.
作者姓名:夏玲玲  魏伟  林辉  周典  钱浩  赵岷  吴永贵
作者单位:1. 安徽医科大学第一附属医院感染病科,合肥,230022
2. 安徽医科大学第一附属医院临床药理研究所,合肥,230022
3. 安徽医科大学第一附属医院肾脏内科,合肥,230022
基金项目:安徽省自然科学基金,安徽省跨世纪学术与技术带头人基金
摘    要:目的 探讨灯盏花素对糖尿病大鼠肝脏保护作用。方法 建立STZ诱导的糖尿病模型 ,随机分 4组 :对照组、模型组、灯盏花素给药组、维生素E给药组 ,每组 10只 ,观察8wk。应用分光光度法检测肝组织MDA含量及SOD、CAT与GSH PX活性 ;HE染色对肝组织作病理检查 ;油红O染色观察肝组织脂肪浸润 ;肝组织ED1(单核 巨噬细胞表面标志 )免疫组织化学采用SABC技术。结果 灯盏花素给药组对糖尿病大鼠血糖、体重无明显影响 ,维生素E给药组可降低血糖 ,延缓体重下降。HE染色模型组部分肝细胞脂肪变性 ;各给药组对肝细胞保护效果较好。模型组肝细胞油红O染色评分为 2 11± 0 82 ,对照组为 0 35± 0 15 ,相比差异有显著性 (P <0 0 1) ;灯盏花素给药组评分为 0 75± 0 6 6 ,维生素E给药组评分为 1 13± 0 78,与模型组相比差异均有显著性 (P均 <0 0 1)。模型组肝组织MDA含量明显升高 ,SOD、CAT、GSH PX活性明显降低 ,各给药组均可降低肝组织MDA含量 ,提高SOD、CAT与GSH PX活性。免疫组织化学显示各给药组均能抑制糖尿病肝组织单核 巨噬细胞浸润的增加。结论 灯盏花素对糖尿病大鼠肝脏保护作用机制部分与抑制肝内脂肪浸润、氧化应激及巨噬细胞浸润有关。

关 键 词:糖尿病  肝脏  氧化应激  灯盏花素  维生素E
文章编号:1001-1978(2004)06-0664-05
修稿时间:2004年2月9日

Experimental study on protective effect of breviscapine in the liver of diabetic rats
XIA Ling-Ling,WEI Wei,LIN Hui,ZHOU Dian,QIAN Hao,ZHAO Min,WU Yong-Gui.Experimental study on protective effect of breviscapine in the liver of diabetic rats[J].Chinese Pharmacological Bulletin,2004,20(6):664-668.
Authors:XIA Ling-Ling  WEI Wei  LIN Hui  ZHOU Dian  QIAN Hao  ZHAO Min  WU Yong-Gui
Abstract:AIM To study protective effect of breviscapine in the liver of diabetic rats. METHODS Diabetes was induced by injection of streptozotocin. Rats were randomly separated into four groups: control group, model group, model group treated with breviscapine and model group treated with vitamin E. 8 wks after STZ injection, the levels of MDA and activities of SOD, CAT as well as GSH-PX in liver tissue were determined by spectrophotometric method. Liver lesions were evaluated using HE staining. Liver fatty changes were evaluated with oil red O staining. Immunohistochemistry for ED1 (monocytes/macrophage marker) was performed by SABC technique.RESULTS Breviscapine could not prevent the decline in body weight (BW) and rise in plasma glucose (BG), Vitamin E could significantly ameliorate the decline in BW and rise in BG in diabetic rats. Light microscopy in HE staining showed that the liver from diabetic animals presented sporadic areas of hepatocytes with fatty degeneration. Breviscapine and Vitamin E group showed minor fatty degeneration in liver tissue. In the diabetic group, the presence of cytoplasmic lipid deposits was confirmed by oil red O staining. In the breviscapine group, these changes were significanly lower than those in the diabetic group. Similar results were obtained in vitamin E group. Liver tissue level of MDA in diabetic rats was higher than those of the control group, breviscapine or Vitamin E administration reduced lipid peroxidation significantly compared with the diabetic group. SOD, CAT, and GSH-PX activities were significantly reduced in the liver of the diabetic group compared with control values. Breviscapine or vitamin E administration all increased SOD, CAT and GSH-PX activities. Liver from diabetic group presented monocytes/ macrophages (ED1 positive cell) infiltration, breviscapine or vitamin E administration all reduced monocytes / macrophages infiltration. CONCLUSION The mechanism of protective effect of breviscapine may be at least partly correlated with suppression on increased oxidative stress and lipid accumulation as well as macrophage infiltration in liver in diabetic rats
Keywords:diabetes  liver  oxidative stress  breviscapine  vitamin E
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