Molecular biology reports · 2026
Salidroside alleviates sepsis-associated acute lung injury through modulation of the ERK/FoxO3a signaling axis and improvement of impaired autophagic flux.
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Ma Xiangli, Zhang Yurong, Huang Zhenzhen, Zhang Ling, Lin Yujie, Fu Xu, Li Peiwu
Аннотация
BACKGROUND: Sepsis-associated acute lung injury (ALI) is a major cause of mortality, and its underlying molecular mechanisms remain incompletely understood. Impaired autophagic flux is considered an important pathological event in this process. Salidroside (Sal), a natural bioactive compound, exhibits anti-inflammatory and cytoprotective effects; however, its role in sepsis-associated ALI requires further investigation.
METHODS: Network pharmacology and molecular docking were employed to identify potential targets and explore candidate signaling pathways. In vitro and in vivo models of sepsis-associated ALI were established using lipopolysaccharide (LPS)-treated RLE-6TN cells and cecal ligation and puncture (CLP) in rats, respectively. Western blotting, immunofluorescence, Ad-mCherry-GFP-LC3B assay, transmission electron microscopy, and JC-1 staining were performed to assess the ERK/FoxO3a signaling pathway, autophagic flux, and mitochondrial function. Phorbol 12-myristate 13-acetate (PMA), an ERK activator, was used for mechanistic validation.
RESULTS: Network pharmacology analysis suggested that the ERK/FoxO3a signaling axis may be involved in the effects of Sal. Experimental results showed that Sal reduced inflammatory responses and attenuated lung injury in both in vitro and in vivo models. Sepsis was associated with impaired autophagic flux, as indicated by increased LC3-II/LC3-I ratio and p62 accumulation, whereas Sal treatment decreased p62 levels and promoted autolysosome formation, suggesting improvement of impaired autophagic flux. In addition, Sal reduced ERK phosphorylation and was associated with increased nuclear localization of FoxO3a. PMA partially attenuated the effects of Sal on ERK/FoxO3a-related changes, autophagy-associated markers, and mitochondrial function.
CONCLUSIONS: Salidroside exerts protective effects in sepsis-associated ALI, which may be associated with modulation of the ERK/FoxO3a signaling axis, improvement of impaired autophagic flux, and maintenance of mitochondrial function.
METHODS: Network pharmacology and molecular docking were employed to identify potential targets and explore candidate signaling pathways. In vitro and in vivo models of sepsis-associated ALI were established using lipopolysaccharide (LPS)-treated RLE-6TN cells and cecal ligation and puncture (CLP) in rats, respectively. Western blotting, immunofluorescence, Ad-mCherry-GFP-LC3B assay, transmission electron microscopy, and JC-1 staining were performed to assess the ERK/FoxO3a signaling pathway, autophagic flux, and mitochondrial function. Phorbol 12-myristate 13-acetate (PMA), an ERK activator, was used for mechanistic validation.
RESULTS: Network pharmacology analysis suggested that the ERK/FoxO3a signaling axis may be involved in the effects of Sal. Experimental results showed that Sal reduced inflammatory responses and attenuated lung injury in both in vitro and in vivo models. Sepsis was associated with impaired autophagic flux, as indicated by increased LC3-II/LC3-I ratio and p62 accumulation, whereas Sal treatment decreased p62 levels and promoted autolysosome formation, suggesting improvement of impaired autophagic flux. In addition, Sal reduced ERK phosphorylation and was associated with increased nuclear localization of FoxO3a. PMA partially attenuated the effects of Sal on ERK/FoxO3a-related changes, autophagy-associated markers, and mitochondrial function.
CONCLUSIONS: Salidroside exerts protective effects in sepsis-associated ALI, which may be associated with modulation of the ERK/FoxO3a signaling axis, improvement of impaired autophagic flux, and maintenance of mitochondrial function.