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[1]易文明 孙文 郭翔宇 吕翠岩 刘铜华.糖痹康对糖尿病周围神经病变大鼠氧化应激及细胞凋亡的影响[J].环球中医药,2015,8(07):798-802.[doi:doi:10.3969/j.issn.1674-1749.2015.07.010]
　YI Wen-ming,SUN Wen,GUO Xiang-yu,et al.Effects of Chinese herbal compound Tangbikang on oxidative stress and apoptosis in rats with diabetic peripheral neuropathy[J].,2015,8(07):798-802.[doi:doi:10.3969/j.issn.1674-1749.2015.07.010]
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糖痹康对糖尿病周围神经病变大鼠氧化应激及细胞凋亡的影响()
     
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《环球中医药》[ISSN:1006-6977/CN:61-1281/TN]

卷:
第8卷
期数:
2015年07期
页码:
798-802
栏目:
论著
出版日期:
2015-07-06

文章信息/Info

Title:
Effects of Chinese herbal compound Tangbikang on oxidative stress and apoptosis in rats with diabetic peripheral neuropathy
作者:
易文明 孙文 郭翔宇 吕翠岩 刘铜华
100078 北京中医药大学东方医院内分泌科(易文明、郭翔宇); 北京中医药大学研究生院(孙文、刘铜华); 首都医科大学附属北京中医医院肾内科(吕翠岩)
Author(s):
YI Wen-ming;  SUN Wen;  GUO Xiang-yu;  et al.
Department of Endocrinology, Dongfang Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100078,China.
关键词:
糖痹康;  糖尿病性周围神经病变;  坐骨神经;  氧化应激;  细胞凋亡
Keywords:
Chinese herbal compound Tangbikang;  Diabetic peripheral neuropathy;  Sciatic nerve;  Oxidative stress;  Apoptosis
分类号:
R285.5
DOI:
doi:10.3969/j.issn.1674-1749.2015.07.010
文献标志码:
A
摘要:
目的 观察糖痹康对糖尿病性周围神经病变大鼠相关的活性氧簇(reactive oxygen species, ROS)、丙二醛(malondialdehyde,MDA)、超氧化歧化酶(superoxide dismutase, SOD)、半胱天冬酶-3(caspas-3)、坐骨神经细胞凋亡的影响,探讨其对氧化应激及细胞凋亡作用的神经保护机制。 方法 使用60只高脂饲料喂养后小剂量链脲佐菌素(streptozotoin,STZ)腹腔注射而诱发的2型糖尿病大鼠动物模型,8周造模成功后按体重随机分为模型组,α-
Abstract:
Objective To observe the effects of Chinese herbal compound Tangbikang on ROS, MDA, SOD, caspas-3, sciatic nerve cell apoptosis in rats with diabetic peripheral neuropathy, and to explore its neuroprotective mechanism against oxidative stress and apoptosis. Methods 60 high fat forage and small dose of streptozotocin intraperitoneal injection induced animal models of type 2 diabetic rats, after 8 weeks, were randomly divided into model group, alpha lipoic acid group, Tangbikang low, medium and high dose groups according to body weight. Another 10 normal rats were set as normal group. Rats in model group and normal group were given distilled water, while Tangbikang groups and alpha lipoic acid group were treated with different doses of Tangbikang and alpha lipoic acid by gastric perfusion. Body weight and fasting blood glucose were measured every 4 weeks, one side of sciatic nerve of rats was taken out after 16 weeks, to detect ROS(colorimetric method), MDA(thiobarbituric acid method), SOD(Xanthine oxidase method). Enzyme-linked immune adsorption method was used to detect the caspas-3 protein expression and TUNEL method to detect apoptosis. Results Compared with the normal group, SOD level was significantly decreased, MDA, ROS levels were significantly increased, the expression level of Caspase-3 protein was significantly increased, and TUNEL positive cells increased significantly in the other groups. Compared with the model group, in the alpha lipoic acid group and Tangbikang high dose group, ROS, MDA levels were significantly decreased, SOD content increased obviously(P<0.05), with no statistical significance between the two groups. TUNEL detection of alpha lipoic acid group and Tangbikang high dose group compared with model group, the number of positive cells decreased(P<0.05). Comparison of Tangbikang high dose group and alpha lipoic acid group, the number of positive cells was slightly more than alpha lipoic acid group(P<0.05). Expression of protein Caspase-3 in alpha lipoic acid group and Tangbikang high dose group in sciatic nerve tissue was significantly less than in the model group(P<0.05), but there was no significant difference between the two groups(P>0.05). Conclusion The Chinese herbal compound Tangbikang can relieve the oxidative stress injury of diabetic peripheral neuropathy, reduce the apoptosis of nerve cells, and delay the development of DPN by improving SOD level and removing overabundant MDA, ROS.

参考文献/References:

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备注/Memo

备注/Memo:
作者简介: 易文明(1980- ),博士,主治医师。研究方向:糖尿病及其并发症临床及机制研究。E-mail:yiwenming33@sina.com 通讯作者:刘铜华( 1963- ),博士,博士后,教授,主任医师,博士生导师。研究方向: 糖尿病及其并发症临床及机制研究。E-mail: Tonghualin@tom.con
更新日期/Last Update: 1900-01-01