@article{Huang_Li_Xu_Song_Xu_Lan_Liu_2022, title={Buyuan decoction inhibits autophagy in a rat model of chronic obstructive pulmonary disease}, volume={74}, url={https://www.serbiosoc.org.rs/arch/index.php/abs/article/view/7207}, DOI={10.2298/ABS211104047H}, abstractNote={<p><strong>Paper description:</strong></p> <ul> <li>Drugs used in chronic obstructive pulmonary disease (COPD) treatment exhibit side effects. Autophagy participates in COPD regulation. Exposure to cigarette smoke causes COPD initiation and progression and increased expression of autophagy markers.</li> <li>The mechanism of Buyuan decoction treatment on autophagy in COPD was investigated in an experimental model in Sprague-Dawley rats in which COPD was induced by lipopolysaccharide injection and cigarette smoke exposure.</li> <li>Buyuan decoction suppresses autophagy in COPD by regulating the expression of autophagy-related proteins LC3-II/I, BNIP-1, ATG7 and p62, and inhibiting PI3K pathway activation.</li> <li>The findings contribute to a novel therapeutic approach for COPD.</li> </ul> <p><strong>Abstract:</strong> Efforts have been made to find a better therapeutic approach with fewer side effects in treating chronic obstructive pulmonary disease (COPD). This study investigated the effect of Buyuan decoction (BYD) on autophagy in COPD rats. An experimental model with Sprague-Dawley rats was established by lipopolysaccharide (LPS) injection and cigarette smoke exposure. Rats were randomly allocated into blank control (normal control), experimental model, low-dose BYD (8.0 g/kg/day), medium-dose BYD (16.0 g/kg/day), high-dose BYD (32.0 g/kg/day) and 3-MA (methyladenine) groups (6 rats/group). Cell and tissue morphology were observed using hematoxylin and eosin staining. Autophagic vesicles were examined with a transmission electron microscope. Protein expression of LC3-II/I, BNIP-1, ATG7, p62, PI3K and p-PI3K in lung tissue was detected by Western blotting. Compared with the experimental model group, the inflammatory infiltrate in lung tissue was reduced, the nuclei of the pulmonary epithelial cells were restored to normal, and the expression of LC3, BNIP1, ATG7 and p-PI3K was significantly downregulated, while p62 expression was significantly upregulated after treatment with the BYD. The effect was most significant in the low-dose BYD group (P<0.05, all groups). These findings suggest that the BYD inhibits the occurrence of autophagy in the pathogenesis of COPD and that it can be a potential treatment.</p>}, number={1}, journal={Archives of Biological Sciences}, author={Huang, Chunyan and Li, Shaofeng and Xu, Chao and Song, Wenlong and Xu, Lei and Lan, Zhihui and Liu, Liangji}, year={2022}, month={Apr.}, pages={5–14} }