ArticleScientific reports2025
Exploring the effect and mechanism of baicalin on sepsis-induced acute lung injury based on network pharmacology and experimental verification.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Baicalin: A comprehensive review of its molecular mechanisms and pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Dietary baicalin supplementation enhances growth performance in fattening Hu sheep via dual modulation of immunity and gastrointestinal microbiome-metabolic crosstalk.Journal of animal science and biotechnology · 2026Article
- Fenofibrate Mitigates Acute Lung Injury in a Rat Model of Feces-Induced Peritonitis.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Baicalin (BA) is an active component of the natural plant Scutellaria baicalensis, which has been used over many years to treat inflammation and respiratory infections. In this study, the sepsis-induced acute lung injury (ALI) mouse model, network pharmacology and molecular docking were used to predict and explore the potential targets and signaling pathways of BA against ALI. The results showed that BA inhibited the major characteristics of ALI, including pathological changes, alveolar-capillary barrier dysfunction, increased inflammatory response and M1 macrophage polarization. Based on network pharmacology and molecular docking analyses, the PI3K/AKT/NF-κB pathway might be an important mechanism by which BA mitigated sepsis-induced ALI. Moreover, BA attenuated the phosphorylation of PI3K, AKT, IκB and NF-κB in the lung tissues of the ALI mice. In conclusion, this study demonstrated that BA ameliorated lung injury in mice, and depressed M1 macrophage polarization through inhibition of the PI3K/AKT/NF-κB pathway.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.