中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (11): 2087-2090.doi: 10.3969/j.issn.1673-8225.2011.11.046

• 组织构建与中医药 tissue construction and traditional Chinese medicine • 上一篇    

慢性阻塞性肺疾病模型大鼠肺组织基质金属蛋白酶9及组织金属蛋白酶抑制剂1与固本颗粒胶囊

杨晓萍1，周兆山2，胡海波2，王平丽1，殷 彬3   

  1. 1青岛大学医学院中西医结合临床专业，山东省青岛市  266021
    2青岛市海慈医疗集团呼吸内科，山东省青岛市  266033
    3山东中医药大学中医内科专业，山东省青岛市  266033
  • 收稿日期:2010-12-10 修回日期:2011-02-15 出版日期:2011-03-12 发布日期:2011-03-12
  • 通讯作者: 周兆山，教授，博士生导师，青岛市海慈医疗集团呼吸内科，山东省青岛市 266033
  • 作者简介:杨晓萍★，女，1985年生，山东省泰安市人，回族，青岛大学在读硕士，主要从事呼吸系统疾病方面的研究。
  • 基金资助:

    青岛市科技发展计划课题， 编号：05-2-NS-41。

Effects of Gubenkeli capsule on matrix metallopeptidase 9 and tissue inhibitor of metalloproteinase1 levels in lung tissue of a rat model of chronic obstructive pulmonary disease

Yang Xiao-ping1, Zhou Zhao-shan2, Hu Hai-bo2, Wang Ping-li1, Yin Bin3   

  1. 1Clinical Department of Chinese and Western Integrative Medicine, Qingdao University Medical College, Qingdao   266021, Shandong Province, China
    2Department of Respiratory Medicine, Hiser Medical Group, Qingdao   266010, Shandong Province, China
    3Internal Medicine Department of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250014, Shandong Province, China
  • Received:2010-12-10 Revised:2011-02-15 Online:2011-03-12 Published:2011-03-12
  • Contact: Zhou Zhao-shan, Professor, Doctoral supervisor, Department of Respiratory Medicine, Hiser Medical Group, Qingdao 266010, Shandong Province, China sunnystar005@163. com
  • About author:Yang Xiao-ping★, Studying for master’s degree, Clinical Department of Chinese and Western Integrative Medicine, Qingdao University Medical College, Qingdao 266021, Shandong Province, China yangxiaoping8501@163.com
  • Supported by:

    Science and Technology Development Program of Qingdao, No. 05-2-NS-41*

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摘要：

背景: 中医药防治慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)的有效性和安全性已初步得到临床认证。
目的：观察COPD模型大鼠肺组织中基质金属蛋白酶9及其特异性抑制物组织金属蛋白酶抑制剂1表达与固本颗粒胶囊干预的影响。
方法：将50只Wistar大鼠随机等分为5组，除正常组外，其余大鼠均以烟熏及气管内滴注脂多糖的方式建立COPD模型。造模   29 d，泼尼松组、固本颗粒胶囊低、高剂量组分别灌胃给予醋酸泼尼松            1.04 mg/(kg•d)，固本颗粒胶囊0.47，0.94 g/(kg•d)，1次/d，观察记录大鼠的一般状况。免疫组织化学方法检测大鼠肺组织中基质金属蛋白酶9及组织金属蛋白酶抑制剂1的表达。
结果与结论：COPD大鼠肺组织中基质金属蛋白酶9及组织金属蛋白酶抑制剂1的表达显著增强(P < 0.05)。药物干预后，COPD大鼠的一般状况明显改善，肺组织中基质金属蛋白酶9及组织金属蛋白酶抑制剂1的表达有所降低；其中，醋酸泼尼松的作用最为显著，固本颗粒高剂量次之，低剂量最弱。说明固本颗粒胶囊能以剂量依赖的方式缓解COPD大鼠的临床表现，改善气道重塑，纠正COPD大鼠体内蛋白酶和抗蛋白酶失衡。

关键词: 固本颗粒胶囊, 慢性阻塞性肺疾病, 动物模型, 基质金属蛋白酶9, 组织金属蛋白酶抑制剂1, 肺组织, 大鼠

Abstract:

BACKGROUND: The effectiveness and safety of traditional Chinese medicine treatment for chronic obstructive pulmonary disease (COPD) have been preliminarily approved by clinical practices.
OBJECTIVE: To investigate the effects of Gubenkeli capsule on the protein expression of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase1 (TIMP-1) in lung tissue of COPD model rats.
METHODS: A total of 50 Wistar rats were randomly divided into five groups with 10 rats in each group: normal control, model, prednisone, Gubenkeli capsule-low dose, and Gubenkeli capsule-high dose. COPD rat models were established in all rats with the exception of the normal control rats by smoking and intratracheal instillation of LPS. At 29 days after COPD induction, rats from the prednisone, Gubenkeli capsule-low dose, Gubenkeli capsule-high dose groups were intragastrically administered prednisone (1.04 mg/kg per day), Gubenkeli capsule (0.4, 0.94 g/kg per day), once a day, to observer rat general conditions. Protein expression of MMP-9 and TIMP-1 in the lung tissue was detected by immunohistochemical methods. 
RESULTS AND CONCLUSION: Protein expression of MMP-9 and TIMP-1 in the lung tissue of COPD rats was significantly increased (P < 0.05). After drug intervention, the general conditions of COPD rats were greatly improved, and protein expression of MMP-9 and TIMP-1 in the lung tissue was decreased. Prednisone yields the strongest effects, followed by high-dose Gubenkeli capsule and low-dose Gubenkeli capsule. These findings demonstrate that Gubenkeli capsule alleviates the clinical manifestations of COPD model rats, improve airway remodeling, and correct the imbalance between prolease and antiprotease in a dose-response manner. 

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