Expression of FIZZ1 on lung tissue of cigarette smoking-induced COPD rats and its relationship with airway inflammation
10.3969/j.issn.1000-4718.2018.06.023
- VernacularTitle:FIZZ1在吸烟大鼠COPD模型肺组织的表达及与气道炎症的相关性研究
- Author:
Yi FENG
1
;
Li CHEN
;
Hong LI
;
Su-Mei WANG
;
Zhi-Hong HUANG
;
Yi WU
;
Sheng-Ming LIU
Author Information
1. 暨南大学附属第一医院
- Keywords:
Chronic obstructive pulmonary disease;
FIZZ1;
Airway inflammation;
Interleukin-4;
Tumor nec-rosis factor-α
- From:
Chinese Journal of Pathophysiology
2018;34(6):1101-1108
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the expression of FIZZ1 ( found in inflammatory zone 1) in the lung tissues from smoking-induced chronic obstructive pulmonary disease (COPD) rats and to explore the potential role of FIZZ1 in air-way remodeling in COPD. METHODS:The male Wistar rats (n=70) were used in the study. The rats were randomly di-vided into COPD group and control group. The rat model of COPD was established by inhaling cigarette smoke alone. HE staining was used to observe the pathological changes of the lung tissues for firming the successful modeling. The protein ex-pression of FIZZ1 in the lung tissues at different time points was determined by immunohistochemistry and Western blot. The inflammatory cells in bronchoalveolar lavage fluid (BALF) were counted. The concentrations of interleukin 4 (IL-4) and tumor necrosis factor α (TNF-α) in both BALF and serum were measured by ELISA. RESULTS:HE staining showed that the inflammatory response was chronic in the lung tissues of model group at 20th week and gradually showed pathologi-cal features of COPD. The results of immunohistochemistry and Western blot showed that in the model group, FIZZ1 protein expression was significantly increased (P<0. 05). Total number of inflammatory cells in BALF in the cigarette smoked rats was significantly higher from 4th week (P<0. 05). Within a certain range, compared with the control group, the concen-trations of inflammatory cytokines IL-4 and TNF-α in both BALF and serum were increased in the model group ( P <0.05). CONCLUSIONS:FIZZ1 may be involved in the occurrence and development of COPD with the mechanism of causing infiltration of inflammatory cells and secretion of cytokines.
