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Buyuan decoction inhibits autophagy in a rat model of chronic obstructive pulmonary disease

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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.
Title: Buyuan decoction inhibits autophagy in a rat model of chronic obstructive pulmonary disease
Description:
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.

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