Mechanism responsible for pulmonary fibrosis induced by concomitant chronic smoke exposure and pentoxifylline administration
- VernacularTitle:己酮可可碱诱导吸烟肺纤维化的机制
- Author:
Jinnong ZHANG
;
Zheng WANG
;
Wei SHI
;
Xiaorong WANG
;
Tingting ZHAO
;
Min XIANG
;
Wei FU
- Publication Type:Journal Article
- Keywords:
Pentoxifylline;
Smoking;
Pulmonary emphysema;
Pulmonary fibrosis;
Th1;
Th2
- From:
Chinese Journal of Pathophysiology
1986;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the impact of long-term administration of pentoxifylline (PTX) on morphology and inflammation of the lung in mouse models with chronic exposure of cigarette smoke. METHODS: Male BALB/c mice were randomized into the following four study groups: smoke-exposure only, shamed smoke-exposure, smoke-exposure and PTX administration, shamed smoke-exposure and PTX administration. Animals assigned to smoke-exposure were put inside a chamber twice a day for cigarette smoke exposure. The oral dose of PTX allocated to each mouse was about 20 mg?kg-1?d-1. Animals were sacrificed anaesthetically at day 120. Slices of lung were stained with H&E for pathological analysis. Modified ashcroft pulmonary fibrosis score (mAPFS) was estimated, and IFN-? (a Th1 cytokine), IL-4 (a Th2 cytokine) in broncho-alveolar lavage fluid (BALF) and hydroxyproline in mouse lung tissue were measured by commercial kits of ELISA assay. RESULTS: Lungs in smoke-exposure only group exhibited emphysema-like morphology, low mAPFS (median 1.50, 95%CI 1.25-3.75), lowest hydroxyproline (2.43?0.11) mg/L and lowest ratio of IL-4 to IFN-? (20.3?25.5), whereas lungs in smoke-exposure and PTX interference group exhibited interstitial fibrosis-like morphology, highest mAPFS (4.75, 4.09-5.71), highest hydroxyproline (5.57?0.55) mg/L and highest ratio of IL-4 to IFN-? (70.7?59.9) among the four study groups (P
