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风百散对慢性阻塞性肺疾病大鼠肺组织基质金属蛋白酶-9及金属蛋白酶组织抑制剂-1表达的影响

Effects of Fengbaisan on the expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in lung tissue of rats with chronic obstructive pulmonary disease.

作者信息

Wang Yu, Su Nan-xiang, Chen Ze-qi, Wang Zhe, Zhang Si-fang

机构信息

Department of Traditional Chinese Medicine, the 2nd Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.

出版信息

Chin J Integr Med. 2014 Mar;20(3):224-31. doi: 10.1007/s11655-013-1619-z. Epub 2013 Nov 16.

DOI:10.1007/s11655-013-1619-z
PMID:24242136
Abstract

OBJECTIVE

To observe effects of Fengbaisan (, FBS) on the expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in lung tissue of rats with chronic obstructive pulmonary disease (COPD) and to investigate the preventive and therapeutic mechanisms of FBS.

METHODS

The COPD rat model was established by cigarette smoke exposure and lipopolysaccharide (LPS) intra-tracheal dripping. The histopathological changes of lung tissue was observed via hematoxylin/eosin staining. The expression of MMP-9 and TIMP-1 in lung tissue was measured by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry.

RESULTS

The typical histopathological changes of COPD were displayed in the model group, Ambroxol Hydrochloride group and FBS group, and the pathological lesions in the FBS group were less than those in the model group. The expression of MMP-9 and TIMP-1 in the model group increased significantly compared with those in the normal group (P<0.05). After treatment for successive 28 days, the expression of MMP-9 and TIMP-1 in the FBS group decreased remarkably as compared with the model group (P<0.05).

CONCLUSIONS

FBS can regulate MMP-9/TIMP-1 imbalance to prevent airway and lung parenchyma remodeling process via reducing the expression of MMP-9 and TIMP-1 in the lung tissue of COPD rats, and this may be a possible therapeutic mechanism of FBS on COPD.

摘要

目的

观察风百散(FBS)对慢性阻塞性肺疾病(COPD)大鼠肺组织基质金属蛋白酶-9(MMP-9)和金属蛋白酶组织抑制剂-1(TIMP-1)表达的影响,探讨FBS的防治机制。

方法

采用香烟烟雾暴露联合气管内滴注脂多糖(LPS)建立COPD大鼠模型。通过苏木精/伊红染色观察肺组织的组织病理学变化。采用逆转录聚合酶链反应(RT-PCR)和免疫组织化学法检测肺组织中MMP-9和TIMP-1的表达。

结果

模型组、盐酸氨溴索组和FBS组均出现COPD典型的组织病理学变化,FBS组的病理损伤较模型组轻。模型组MMP-9和TIMP-1的表达较正常组显著升高(P<0.05)。连续治疗28天后,FBS组MMP-9和TIMP-1的表达较模型组明显降低(P<0.05)。

结论

FBS可通过降低COPD大鼠肺组织中MMP-9和TIMP-1的表达来调节MMP-9/TIMP-1失衡,从而预防气道和肺实质重塑过程,这可能是FBS治疗COPD的一种潜在机制。

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