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

机译:腹腔注射香烟烟雾提取物诱发BALB / C小鼠肺气肿以及心肌和骨骼肌损伤

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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.
机译:背景:慢性阻塞性肺疾病(COPD)是一种慢性,进行性气道疾病。为了识别COPD的机制,已经建立了各种类型的COPD动物模型,并且发病机理也不同。本研究旨在通过腹膜内注射BALB / C小鼠香烟烟雾提取物(CSE)建立COPD动物模型。方法:小鼠腹腔注射PBS / CSE并在第28天处死。肺功能,肺组织病理学,心脏和骨骼肌形态,白细胞计数和支气管肺泡灌洗液(BALF)的抗氧化活性,肺实质细胞凋亡指数(AI) ),测定切割的caspase-3的表达,MMP-2和MMP-9 mRNA的表达以及肺组织中MMP-2和MMP-9的活性。结果:腹腔注射CSE引起肺实质破坏,肺功能降低,白细胞计数,心脏和周围肌肉损伤,肺实质AI升高,caspase-3蛋白裂解,MMP-2和MMP-9 mRNA的表达,肺组织中的MMP-2和MMP-9蛋白,并抑制BALF中的抗氧化活性(P <0.05)。结论:腹腔注射CSE可引起小鼠肺气肿,肺实质细胞凋亡以及心肌和骨骼肌损伤。该模型中所有与病理生物学相关的机制均与COPD患者共享。

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