Existence of multiple organ aging in animal model of emphysema induced by cigarette smoke extract.

Guibin Liang,Yingjiao Long,Hongbo Zhang,Yan Chen,Dandan Zong,Huaihuai Peng,Zhihui He

doi:10.18332/tid/143853

Abstract

INTRODUCTIONIt is commonly considered that COPD or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components. However, the issue if there are any aging signs in other organs in patients with COPD or emphysema remains unclear. The aim of this study is to explore whether there is multiple organ aging in the animal model of emphysema induced by cigarette smoke extract (CSE), and to ascertain the possible mechanisms, if any.METHODSThe animal model of emphysema was induced by CSE. Histomorphological changes in lung, heart, liver, kidney and spleen tissues were measured after staining with hematoxylin and eosin (H&E). The concentrations of stem cell factor (SCF), CyclinD1 and superoxide dismutase (SOD) in serum were determined by ELISA kit. The expressions of p16 (INK4a), Sca-1, eNOS proteins and mRNA in lung, heart, liver, kidney and spleen tissues were detected by Western blotting and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), respectively. Decitabine (Dec) was applied to examine whether it could alter the changes caused by CSE.RESULTSThe histomorphology of lung tissue was significantly changed, while other organs exhibited normal structure and histomorphology. The concentrations of SCF, CyclinD1 and SOD in serum were lower in the CSE group than in the control group. The expression levels of p16(INK4a) protein and mRNA in lung, heart, liver, kidney and spleen tissues were higher in the CSE group than in the control group, while the expression levels of Sca-1 and eNOS proteins and mRNA were lower in the CSE group than in the control group, in the tissues described above. Dec could partly alleviate the damages caused by CSE and the degree of alleviation resulted by Dec varied from organ to organ.CONCLUSIONSIn addition to the aging of the lung tissue in the emphysema animal model induced by CSE, the tissues of the heart, liver, kidney and spleen were also in the progress of aging, but the sensibility and affinity of lung to CSE were higher than those of the other organs. Multiple organ aging may also exist in the animal model of emphysema induced by CSE. DEC can partly alleviate the multiple organ aging caused by CSE.

Highlights

INTRODUCTION It is commonly considered thatchronic obstructive pulmonary disease (COPD) or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components
The animal model of emphysema induced by intraperitoneal injection of cigarette smoke extract (CSE) has been verified in previous studies, and it is equivalent to the animal model of emphysema induced by cigarette smoke (CS) exposure in lung function and histomorphology[4]
Quantitative analysis showed that mean linear intercept (MLI) and destructive index (DI) were significantly higher in the CSE group (69.65 ± 10.19 μm, 45.36 ± 6.96%) and CSE+Dec group (53.97 ± 8.86 μm, 35.83 ± 5.75%) than those in the control group (27.69 ± 5.37 μm, 9.95 ± 1.19%) and Dec group (29.17 ± 5.31 μm, 10.36 ± 1.40%) (p

Summary

Introduction

COPD or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components. The aim of this study is to explore whether there is multiple organ aging in the animal model of emphysema induced by cigarette smoke extract (CSE), and to ascertain the possible mechanisms, if any. Aging is characterized by progressive decline in tissue and organ function and increased risk of mortality, which is associated with a wide range of human disorders, including cancer, diabetes, cardiovascular, and neurodegenerative diseases. Some studies have shown that chronic obstructive pulmonary disease (COPD) or at least emphysema was a disease of accelerated lung aging[1]. It is commonly considered that COPD or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components

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