Bufei Tongbi Decoction Inhibits Pulmonary Fibrosis in Diabetic Rats via TGF-β1/p-Smad3 Signaling Pathway
10.13422/j.cnki.syfjx.20241518
- VernacularTitle:基于TGF-β1/p-Smad3信号通路探究补肺通痹汤抑制糖尿病相关性肺纤维化的作用机制
- Author:
Gang WANG
1
;
Rensong YUE
2
;
Qiyue YANG
2
;
Dan ZHANG
1
;
Xin CHEN
1
Author Information
1. Zigong First People's Hospital， Zigong 643000， China
2. Affiliated Hospital of Chengdu University of Traditional Chinese Medicine， Chengdu 610075， China
- Publication Type:Journal Article
- Keywords:
transforming growth factor-β1 （TGF-β1）/phosphorylated Smad family member 3 （p-Smad3） signaling pathway;
Bufei Tongbi decoction;
modified Bufei decoction;
diabetic rats;
pulmonary fibrosis
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(10):176-184
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo study the effect of Bufei Tongbi decoction on pulmonary fibrosis in diabetic rats via the transforming growth factor-β1 （TGF-β1）/phosphorylated Smad family member 3 （p-Smad3） signaling pathway. MethodsStreptozotocin （60 mg·kg-1） and bleomycin （24.80 U·kg-1） were used to prepare the rat model of diabetes with pulmonary fibrosis by intratracheal injection. Sixty rats were randomly assigned into blank， model， low-， medium-， and high-dose （3.98， 7.95， and 15.90 g·kg-1， respectively） Bufei Tongbi decoction， and pirfenidone （0.36 mg·kg-1） groups （n=10）. The successfully modeled rats in each group were administrated with corresponding agents once per day for four consecutive weeks. After drug administration， fasting blood glucose and lung function indicators were measured. Chemical immunoassay was employed to determine the serum levels of hydroxyproline （Hyp）， hyaluronic acid （HA）， and laminin （LN）. The lung index was determined by the wet and dry methods. The pathological changes in the lung tissue were observed by hematoxylin-eosin （HE） staining， and the degree of fibrosis was detected by Masson staining. The mRNA and protein levels of TGF-β1， p-Smad3， Smad3， α-smooth muscle actin （α-SMA）， collagen type Ⅰ alpha 1 （Col1A1）， and fibronectin were determined by PCR and Western blotting， respectively. ResultsCompared with the blank group， the model group showed alveolar septa thickening， obvious thickening of the basement membrane of pulmonary blood vessels， severe destruction of the alveolar structure， structural disarrangement of the lung parenchyma， and an increase in the proportion of inflammatory cell infiltration in the lung tissue， together with a large amount of blue collagen deposition and a large amount of collagen fibroplasia in the bronchial wall， vessel wall， interstitium， and alveolar wall， which indicated severe fibrosis. Bufei Tongbi decoction groups and the pirfenidone group showed lower fasting blood glucose level （P<0.05） and higher forced vital capacity （FVC）， cytoplasmic dynein （Cydn）， FEV0.3/FEV ratio， and lung index （P<0.05） than the model group. Moreover， these groups demonstrated alleviated lung fibrosis， elevated Hyp， HA， and LN levels， down-regulated mRNA levels of α-SMA， Col1A1， and fibronectin， and down-regulated protein levels of TGF-β1， Smad3， p-Smad3， α-SMA， Col1A1， and fibronectin （P<0.05）. ConclusionBufei Tongbi decoction can inhibit pulmonary fibrosis in diabetic rats by inhibiting the TGF-β1/p-Smad3 signaling pathway.
