Mechanisms underlying the effects of Buyang Huanwu Decoction against sepsis-induced ARDS using network pharmacology and experimental validation.

Authors

Wanying Tan, Chun Wang, Xiuxiu Liu, Jiangting Deng, Zhipei Sang, Xiaoyu Hu

Published in

Journal of ethnopharmacology. Pages 122573. Oct 26, 2026. Epub Oct 26, 2026.

Abstract

Buyang Huanwu Decoction (BYHW), a classic formula from Yilin Gaicuo Qing Dynasty, is indicated for stroke in patients with qi deficiency and blood stasis in the Chinese Pharmacopoeia. In traditional Chinese medicine (TCM), the pathogenesis of acute respiratory distress syndrome (ARDS) is associated with qi deficiency, blood stasis, and heat-toxin obstructing the lungs, which align with the therapeutic actions of this formula.
To investigate the effects of BYHW on sepsis-induced ARDS and the mechanisms underlying these effects.
ARDS was induced through LPS treatment in wild-type and eNOS-deficient (eNOS^-/-) mice. The components of BYHW were analyzed using UPLC-UV-MS. Potential associated targets and pathways were predicted by network pharmacology and molecular docking experiments. Relevant protein and mRNA expression levels were assessed by Western blot analysis, immunofluorescence analysis, or qPCR.
BYHW significantly improving the hypothermia, elevated plasma levels of IL-1β, TNF-α, and IL-6, the lung index and injury induced by LPS in wild-type (WT) mice. However, these effects of BYHW were markedly in eNOS^-/- mice. LPS downregulated AQP1 protein expression and upregulated Cav-1 protein expression and the p-P65/P65 ratio in both groups but increased the p-IκB/IκB ratio only in the WT mice. Pretreatment of BYHW increased the expression of eNOS and AQP1, decreased the Cav-1 expression and P65/IκB phosphorylation in WT mice, but the action on the P65/IκB phosphorylation and AQP1 expression were abrogated in eNOS^-/- mice.
BYHW protect against sepsis-induced ARDS may be related to decrease the eNOS-NF-κB-mediated synthesis of inflammatory cytokines and upregulation of AQP1 expression.

PMID:
42933740
Bibliographic data and abstract were imported from PubMed on 27 Oct 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.