Comparison between cigarette smoke-induced emphysema and cigarette smoke extract-induced emphysema

Abstract

Background and objectiveEmphysema is the main pathological feature of COPD and also is the focus of the related research. Although several emphysema animal models have been established, exact comparison of findings is seldom. The present study aimed to compare cigarette smoke (CS) exposure-induced emphysema model and intraperitoneal injection of cigarette smoke extract (CSE)-induced emphysema model to evaluate the effectiveness of the two different modeling methods.MethodsSix-week-old male C57BL/6 J mice were used and randomly divided into two groups: CS exposure and intraperitoneal injection of CSE. Each group was subdivided into two subgroups: control and CS or CSE. Lung function, mean linear intercept (MLI), destructive index (DI), apoptotic index (AI), total and differential cells count in broncholavolar lavage fluid (BALF), SOD and IL-6 concentration in serum were measured.ResultsCompared with their respective controls, lung function was significantly decreased in CS and CSE groups (P < 0.01); MLI, DI, and AI of lung tissue were significantly higher in CS and CSE groups (P < 0.01); total number of leukocytes, the number and percentage of neutrophils (NEUs), and the number of macrophages (MAC) in BALF were significantly higher in CS and CSE groups (P < 0.01); SOD concentration in serum was significantly decreased in CS and CSE groups (P < 0.01); IL-6 concentration in serum was significantly increased in in CS and CSE groups (P < 0.01). There was no significant difference between CS group and CSE group in any of the parameters described above.ConclusionsBoth CS exposure and intraperitoneal injection of CSE could induce emphysema and the effectiveness of the two different modeling methods were equal.

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

“…In addition to the well-known mechanisms in which the chronic inflammation of airways, extracellular matrix destruction and oxidative stress are thought to contribute to the pathogenesis of COPD (3), the apoptosis of structural cells in the lung is recently suggested to be an important upstream event in the pathogenesis of COPD (4)(5)(6)(7)(8)(9). Our previous studies demonstrated that the apoptosis was involved in both alveolar epithelial cells and endothelial cells in the parenchyma of COPD and that the apoptotic cells were increased in emphysematous lung parenchyma in both animal model and patients (10)(11)(12)(13).…”

Ablation of Arf-expressing cells ameliorates cigarette smoke-induced lung dysfunction in mice

“…Similar to the CS exposure, the CSE treatment also leads to impaired pulmonary function [33,34]. We performed pulmonary function tests in CSE-treated mice.…”

l-Menthol alleviates cigarette smoke extract induced lung injury in rats by inhibiting oxidative stress and inflammationvianuclear factor kappa B, p38 MAPK and Nrf2 signalling pathways

“…25 In summary, three cigarettes (Taishan, China Tobacco Shandong Industrial CO. Ltd: tar, 11 mg; nicotine, 1.1 mg; carbon monoxide, 11 mg) were burned and the smoke was collected using a peristaltic pump, and the smoke was nally bubbled into 10 ml of phosphatebuffered saline (PBS, pH 7.4). The CSE was freshly prepared before use and then ltered through a 0.22 mm Millipore lter for removing particles and bacteria.…”

“…[25][26][27] It was revealed that both CS exposure and intraperitoneal injection of CSE could induce rat emphysema and the effectiveness of the two different modelling methods was equal. 25 However, intraperitoneal injection of CSE is more convenient in operation rather than cigarette smoke exposure daily.…”

“…Previous study indicated that intraperitoneal injection of CSE was a new convenient method for rat emphysema modelling, which showed no signicant difference from typical cigarette smoking exposure method. 25 All HE stained lung tissue slices were observed under light microscope (100Â). As shown in Fig.…”