Evidence map›Paper›PMID 41049072›Full record

ArticleJournal of inflammation research2025

Dual Effects of Sodium Houttuyfonate Against Acute Rhinosinusitis: Antibacterial Action and Epithelial Barrier Repair Through the p38 MAPK/ERK Pathway.

Yang Fang, Huixia Zhou, WeiYi Li, Lu Bai, Xinchen Sun, KaiYuan He, Shanshan Xue, Yongjun Wu

Abstract read
In one paragraph

Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Yang FangDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
Huixia ZhouDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
WeiYi LiDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
Lu BaiDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
Xinchen SunDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
KaiYuan HeDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
Shanshan XueDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
Yongjun WuDepartment of Otolaryngology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Methods: Network pharmacology was applied to identify SH-associated targets and pathways. An ARS rat model was induced by inserting Staphylococcus aureus-soaked Merocel sponges into the nasal cavity. Rats received low, medium, or high doses of SH, with control and positive drug groups. Symptom scoring, CT, histopathology, hematology, ELISA, qRT-PCR, and immunohistochemistry were conducted. In vitro, human nasal epithelial cells (HNEpCs) were stimulated with lipopolysaccharide (LPS) and treated with SH, with or without MAPK modulators SB203580 (inhibitor) or Anisomycin (activator). Cell viability, cytokine expression, and ERK/p38 MAPK phosphorylation were assessed. Results: SH improved nasal symptoms, reduced epithelial injury, and normalized nasal pH in ARS rats. It downregulated IL-1β, IL-6, TNF-α, and ICAM-1 while upregulating IL-4. Transmission electron microscopy showed restoration of ciliary and mitochondrial integrity. In HNEpCs, 60 μM SH was optimal by CCK-8 assay. In LPS-stimulated cells, SH suppressed IL-1β/IL-6 mRNA and inhibited ERK and p38 MAPK phosphorylation; these effects were reversed by Anisomycin, confirming pathway involvement. Conclusion: SH alleviates sinonasal inflammation in ARS by inhibiting bacterial activity and restoring epithelial integrity through p38 MAPK/ERK suppression. These findings support SH as a potential therapy for upper airway inflammatory diseases.

Indexed as

acute rhinosinusitisethnopharmacologyhouttuynia cordatainflammationp38 MAPK/ERK signalingsodium houttuyfonate

Identifiers

PMID41049072
PMCPMC12493869

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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.