TGF - Β RECEPTOR INHIBITORS AFFECT THE PROLIFERATION OF CHRONIC OBSTRUCTIVE PULMONARY FIBROBLASTS BY REGULATING THE EXPRESSION OF GROWTH FACTORS

Akira Miyamoto¹, Chimi Miyamoto², CaiJu Huang³, Zhiming Tang⁴, Zhongli Wang⁵, Hua Wu⁵, Minxing Gao⁶, Yichao Wang⁷, Liang Tao⁸, lvyu Zhao⁹, Delian An¹⁰, Chi Zhang^{11, *}

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

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.