Authors

Akira Miyamoto1, Chimi Miyamoto2, CaiJu Huang3, Zhiming Tang4, Zhongli Wang5, Hua Wu5, Minxing Gao6, Yichao Wang7, Liang Tao8, lvyu Zhao9, Delian An10, Chi Zhang11, *


Departments

1Department of Faculty Rehabilitation, Kobe International University, Kobe, 6580032, Japan - 2Department of Health and Medical Sciences, Aino University, Ibaragi, 5670012, Japan - 3Department of Rehabilitation, NanAo People's Hosptial, ShenZhen, 518121, PR China - 4Department of Rehabilitation Medicine, The Third Affiliated Hospital of Sun Yet-sen University, Guangzhou 510630, PR China - 5The Rehabilitation Center of Jia Xing Second Hospital, Jiaxing 314001, PR China - 6Department of Rehabilitation, Shengjing Hospital of China Medical University, Shenyang 117004, PR China - 7Department of Rehabilitation, Jining Integrated Chinese and Western Medicine Hospital, Jining 272000, PR China - 8Department of Neuro Rehabilitation, Ningbo Rehabilitation Hospital, Ningbo 315000, PR China - 9Department of Rehabilitation Medicine, The Third Affiliated Hospital of Sun Yet-sen University, Guangzhou 510630, PR China - 10Department of Rehabilitation Medicine, The Third Affiliated Hospital of Sun Yet-sen University, Guangzhou 510630, PR China - 1Department of Rehabilitation Medicine, Affiliated Hospital of Southwest Medical University, Luzhou 646000, PR China

Abstract

Objective: To analyze the effect of TGF - β receptor inhibitors on the proliferation of COPD fibroblasts by regulating the expression of growth factors. 

Methods: Twenty-four healthy male SD rats were randomly divided into a normal group, a model group, and a TGF - β receptor inhibitor group, with 8 rats in each group. Every group except the normal one used the cigarette smoke inhalation method to establish the rat COPD model. After the model was established successfully, the TGF - β receptor inhibitor was dissolved in 5ml of normal saline and given to the rats in the TGF - β receptor inhibitor group for atomization inhalation treatment. The normal group rats in the model group and the model group were given the same volume of saline atomization inhalation. Changes in lung tissue morphology, TGF - β 1, and bFGF were observed, and the proliferation and apoptosis of fibroblasts were compared. 

Results: Compared with the model group, the bronchociliary structure of the TGF - β receptor inhibitor group was complete, and the infiltration of inflammatory cells in the alveoli was slightly relieved. The level of TGF - β 1 and bFGF in the model group’s lung tissue was significantly higher than that of the normal group (P<0.05), and the level of TGF - β 1 and bFGF in the TGF - β receptor inhibitor group’s lung tissue was lower than that of the model group (P<0.05). The proliferation activity of fibroblasts in the model group was significantly higher than that of the normal group (P<0.05). The proliferation activity of fibroblasts in the TGF - β receptor inhibitor group was significantly lower than that of the model group (P<0.05). The apoptosis index of fibroblasts in the model group was significantly higher than that of the normal group (P<0.05). The apoptosis index of fibroblasts in the TGF - β receptor inhibitor group was significantly higher than that of the model group (P<0.05). 

Conclusion: TGF - β receptor inhibitors can significantly inhibit the proliferation and promote the apoptosis of fibroblasts in COPD rats. The mechanism may be related to the regulation of TGF - β 1, bFGF, and other growth factors.

Keywords

TGF - β receptor inhibitor, growth factor, COPD, fibroblast, proliferation.

DOI:

10.19193/0393-6384_2021_1_26