Mechanism of Buyang huanwu tang in improving idiopathic pulmonary fibrosis by delaying cellular senescence
- VernacularTitle:补阳还五汤延缓细胞衰老改善特发性肺纤维化的机制研究
- Author:
Long CHEN
1
;
Jinglian QU
1
Author Information
1. College of Basic Traditional Chinese Medicine，Guizhou University of Traditional Chinese Medicine，Guiyang 550025，China
- Publication Type:Journal Article
- Keywords:
Buyang huanwu tang;
idiopathic pulmonary fibrosis;
cellular senescence;
TGF-β1/Smad signaling pathway
- From:
China Pharmacy
2025;36(10):1186-1190
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the improvement effect and mechanism of Buyang huanwu tang on idiopathic pulmonary fibrosis （IPF） model rats. METHODS The rats were randomly divided into normal group， model group， pirfenidone group （positive control， 0.162 g/kg）， Buyang huanwu tang low-， medium- and high-dose groups （6.435， 12.87， 25.74 g/kg）， with 6 rats in each group. Except for the normal group， IPF model was established in the remaining groups by intratracheal injection of bleomycin sulfate. On the second day after successful modeling， medication was administered once a day for 28 consecutive days. After the last medication， the appearance and morphology， pathological changes， and fibrosis status of the lung tissues in rats were observed. cyclin-dependent kinase inhibitor 2A （P16）， P21， transforming growth factor-β1 （TGF-β1）， Smad3， Smad7， epidermal growth factor （EGF）， epidermal growth factor receptor （EGFR）， matrix metalloproteinase 12 （MMP-12）， chemokine ligand 2 （CCL2） and interleukin-4 （IL-4） protein expression in lung tissue were all determined. RESULTS Compared with the normal group， the lung tissue of rats in the model group exhibited gray-white color， harder texture， obvious bruising and cysts. Additionally， alveolar septa were significantly thickened， their structural integrity severely compromised， accompanied by pronounced infiltration of inflammatory cells and severe pulmonary fibrosis. Collagen volume fraction， protein expressions of P16， P21， TGF-β1， Smad3， EGF， EGFR and （IL-4） in lung tissue significantly increased （P＜0.05 or P＜0.01）， while Smad7， MMP-12 and CCL2 protein expressions were significantly decreased （P＜0.05 or P＜0.01）. Compared with the model group， the appearance， pathological morphology， and fibrosis degree of rat lung tissue in Buyang huanwu tang groups were significantly improved， and the above quantitative indicators were significantly reversed （P＜0.05 or P＜0.01）. CONCLUSIONS Buyang huanwu tang can ameliorate IPF in rats， and its underlying mechanism may be associated with the inhibition of TGF-β1/Smad signaling pathway activity and the attenuation of cellular senescence.
