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

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

doi:10.18332/tid/143853

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

Tob Induc Dis. 2022 Jan 17:20:02. doi: 10.18332/tid/143853. eCollection 2022.

Authors

Guibin Liang¹, Zhihui He¹, Yan Chen², Hongbo Zhang³, Huaihuai Peng⁴, Dandan Zong², Yingjiao Long²

Affiliations

¹ Department of Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha, China.
² Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, China.
³ Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, China.
⁴ Department of Intensive Care Unit, The Second Xiangya Hospital, Central South University, Changsha, China.

Abstract

Introduction: It 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.

Methods: The 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.

Results: The 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.

Conclusions: In 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.

Keywords: aging; cigarette smoke; decitabine; emphysema; multiple organs.