ArticleJournal of molecular histology2025
Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in Staphylococcus aureus pneumonia.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The impact of traditional Chinese medicine on gastrointestinal dysfunction in sepsis patients: a systematic review and network meta-analysis.Frontiers in pharmacology · 2025Pooled it
- A comprehensive review of regulatory mechanisms of novel enterotoxin genes inAnnals of medicine · 2026Review
- Apigenin mitigates intestinal barrier dysfunction in sepsis by modulating the AKT signaling pathway.BMC gastroenterology · 2025Article
- Oleaceae plants: a source of metabolites with atheroprotective potential.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundS. aureus pneumonia, one of the most common S. aureus-induced diseases, is characterized by infectious inflammation in alveoli, distal airway, and lung interstitial. Forsythiaside A possesses anti-inflammatory, anti-infective, and other pharmacological properties in several diseases. The role of forsythiaside A remains unclear in S. aureus pneumonia. AIM OF THE STUDY: We aimed to figure out the role of forsythiaside A in S. aureus pneumonia.
methodsRAW264.7 cells and C57BL6 mice were infected with S. aureus to construct S. aureus pneumonia cell model and animal model, respectively. A series of experiments including MTT, ELISA, Western blot, H&E staining and EBD staining were operated to figure out the role of forsythiaside A in S. aureus pneumonia.
resultsIn RAW264.7 cells, forsythiaside A did not induce cell toxicity but triggered cytokines (TNF-α, IL-6 and IL-1β) release in a dose-dependent manner. Moreover, forsythiaside A inhibited p38 JNK/MAPK/ERK and NF-κB pathways by repressing phosphorylation of p38, JNK, ERK and p65 proteins. For in vivo study, forsythiaside A improved survival rate of S. aureus pneumonia mice by alleviating lung injury. In addition, forsythiaside A protected from air-blood barrier destruction and pulmonary edema. At last, forsythiaside A inhibited neutrophils infiltration and inflammatory response in bronchoalveolar lavage fluid.
conclusionsForsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in S. aureus pneumonia, which provided a novel insight for S. aureus pneumonia treatment.
Indexed as
Identifiers
40293580What 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.