Intraperitoneal injection of cigarette smoke extract induced emphysema, and injury of cardiac and skeletal muscles in BALB/C mice

Intraperitoneal injection of cigarette smoke extract induced emphysema, and injury of cardiac and skeletal muscles in BALB/C mice
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腹腔注射香烟烟雾提取物致 BALB/C 小鼠肺气肿及心肌和骨骼肌损伤

DOI:
10.3109/01902148.2012.745910
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发表时间:
2013-02-01
影响因子:
1.7
通讯作者:
Wu, Shang-jie
Wu, Shang-jie
中科院分区:
医学4区
文献类型:
--
作者:
Zhang, Yan;Cao, Jun;Wu, Shang-jie

文献摘要

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摘要背景:慢性阻塞性肺疾病(COPD)是一种慢性、进行性气道疾病。为了认识COPD的发病机制,人们建立了各种类型的COPD动物模型,其发病机制各不相同。本研究旨在通过腹腔注射香烟烟雾提取物(CSE)建立小鼠COPD动物模型。方法:将小鼠腹腔内注射PBS/CSE,并在第28天处死。检测肺功能、肺组织病理学、心脏和骨骼肌形态学、支气管肺泡灌洗液(BALF)中白细胞计数和抗氧化活性、肺实质细胞凋亡指数(AI)、肺组织中半胱氨酸天冬氨酸蛋白酶-3(caspase-3)表达、MMP-2和MMP-9 mRNA表达、MMP-2和MMP-9活性。结果如下:腹腔注射CSE可引起肺实质破坏、肺功能下降、白细胞计数、心肌和外周肌损伤,肺实质AI、Caspase-3蛋白、MMP-2和MMP-9 mRNA表达、MMP-2和MMP-9蛋白活性升高,BALF抗氧化活性降低(P < 0.05)。结论:腹腔注射CSE可引起小鼠肺气肿、肺实质细胞凋亡及心肌和骨骼肌损伤。该模型中的所有病理生物学相关机制与COPD患者相同。
ABSTRACT Background: Chronic obstructive pulmonary disease (COPD) is a chronic, progressive, airway disease. In order to recognize mechanisms of COPD, various types of COPD animal models have been established, and the pathogenesis are different. The present study was designed to establish a COPD animal model by intraperitoneal injection of cigarette smoke extract (CSE) in BALB/C mice. Methods: Mice were injected intraperitoneally with PBS/CSE and sacrificed at day 28. Pulmonary function, pathology of lung tissue, morphology of hearts and skeletal muscle, leukocytes count and antioxidant activity of bronchoalveolar lavage fluid (BALF), pulmonary parenchymal apoptosis index (AI), expression of cleaved caspase-3, expression of MMP-2 and MMP-9 mRNA, and activity of MMP-2 and MMP-9 in lung tissue were measured. Results: Intraperitoneal injection of CSE induced pulmonary parenchymal destruction, pulmonary function reduction, leukocytes count, injury of cardiac and peripheral muscles, and increased pulmonary parenchymal AI, cleaved caspase-3 protein, expression of MMP-2 and MMP-9 mRNA, activity of MMP-2 and MMP-9 protein in lung tissue, and suppressed antioxidant activity in BALF (P < 0.05). Conclusions: Intraperitoneal injection of CSE produced emphysema, pulmonary parenchymal apoptosis, and injury of cardiac and skeletal muscles in mice. All pathobiologically relevant mechanisms in this model are shared with the COPD patients.