ArticleJournal of natural medicines2026
A novel mechanism for treating acute lung injury with ligustilide: elucidation via network pharmacology and in vitro validation.
Article in Journal of natural medicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Ligustilide inhibits the release of multiple inflammatory factors and alleviates acute lung injury (ALI), although its underlying mechanisms require further investigation. This study combined network pharmacology and in vitro experiments to systematically elucidate the therapeutic mechanism of ligustilide against lipopolysaccharide (LPS)-induced ALI. Potential targets of ligustilide and ALI-related genes were screened from public databases, identifying 227 overlapping targets. Protein-protein interaction (PPI) network analysis revealed PIK3R1 as core targets. KEGG pathway enrichment analysis highlighted the PI3K/Akt/mTOR signaling axis as one of the most significantly enriched pathway (P < 0.001). Molecular docking confirmed a strong binding affinity between ligustilide and the PIK3R1 protein. In vitro, LPS exposure (10 µg/ml, 48 h) suppressed autophagy in HPAEpiCs, evidenced by reduced Beclin-1 and LC3 protein levels and a decrease in autophagic vesicles, while concurrently activating the PI3K/Akt/mTOR signaling pathway (P < 0.01) and elevating the levels of IL-17 A, IL-6, and TNF-α. Treatment with ligustilide (25 µg/ml) significantly reversed these effects by modulating autophagy-related markers and suppressing the release of these inflammatory cytokines (P < 0.05). Furthermore, co-treatment with anti-IL-17 A neutralizing antibodies amplified these protective effects through enhanced inhibition of the PI3K/Akt/mTOR pathway (P < 0.01). These findings suggest that ligustilide alleviates ALI by modulating autophagy-related markers and inhibiting inflammatory responses via the IL-17 A-mediated PI3K/Akt/mTOR signaling pathway. The integration of network pharmacology with experimental validation provides a robust mechanistic framework for understanding ligustilide’s therapeutic potential against ALI.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.