Salvianolic Acid B Inhibits Ferroptosis in Acute Lung Injury: Network Analysis and Experimental Validation.

Authors

Hejun Gao, Renhui Xiong, Na Yue, Jiaxin Wang, Shouyuan Tian

Published in

Journal of cellular and molecular medicine. Volume 30. Issue 17. Pages e71344.

Abstract

This current study aimed to decipher the anti-inflammatory, anti-ferroptosis and pronounced lung-protective activities of Salvianolic acid B (Sal B) by integrating network pharmacology and experimental confirmation across multiple aspects. The optimal target protein and the relevant molecular mechanisms for Sal B in the context of ALI were analysed using network pharmacology. Molecular dynamics simulations and BLI were performed on the core protein ALB-compound Sal B identified through molecular docking. The pharmacological efficacy of Sal B and its underlying mechanisms were further substantiated through both in vitro and in vivo experiments, utilizing the LY294002 inhibitor and si-ALB to confirm the involvement of ALB as a target. Additionally, RNA sequencing of murine lung tissues was conducted to further elucidate the molecular mechanism of Sal B. The results of network pharmacology indicated that a total of 155 potential target genes through which Sal B may exert its protective effects against ALI were identified, with essential pathways including PI3K-AKT, TNF and IL-17 signalling pathways. Molecular docking, MD, and BLI demonstrated stable binding between Sal B and the core target ALB. In vitro and in vivo evidence confirmed that Sal B attenuates LPS-induced ALI by inhibiting ferroptosis via the PI3K/AKT axis, as corroborated by LY294002 and si-ALB intervention. RNA sequencing and network pharmacological analysis synergistically revealed the PI3K/AKT pathway as a potential signalling pathway for Sal B. Sal B ameliorates sepsis-induced ALI via a defined mechanism that involves the activation of the PI3K-AKT pathway, thereby inhibiting ferroptosis both in vivo and in vitro.

PMID:
42693654
Bibliographic data and abstract were imported from PubMed on 04 Sep 2026.

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