ArticleJournal of microbiology and biotechnology2025
SHR02 Modulates Inflammatory and Oxidative Stress Responses by Inhibiting NF-κB and Activating Nrf2 in Macrophages and Dendritic Cells.
Article in Journal of microbiology and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Oxidative-Stress-Associated Molecular Signatures in Immune-Mediated Diseases: A Systematic Review Integrating Machine Learning and Systems Biology Approaches.Antioxidants (Basel, Switzerland) · 2026Review
- Mechanisms and clinical research progress of IL-6-mediated crosstalk between the alveolar microenvironment and the immune system in patients with severe pneumonia undergoing mechanical ventilation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SHR02, a derivative of homoisoflavonoid, exhibits potent anti-inflammatory activity in innate immune cells. In this study, we investigated the immunomodulatory effects of SHR02 in dendritic cells (DC2.4) and macrophages (RAW 264.7) under Toll-like receptor (TLR) stimulation. SHR02 significantly suppressed the secretion of pro-inflammatory cytokines (TNF-α and IL-6), reduced nitric oxide (NO) and reactive oxygen species (ROS) production, and downregulated the expression of iNOS and COX-2. Mechanistically, SHR02 inhibited NF-κB phosphorylation in dendritic cells while enhancing Nrf2 nuclear translocation in both cell types. These findings suggest that SHR02 modulates inflammatory and oxidative responses through both NF-κB and Nrf2 signaling pathways and may serve as a promising candidate for the treatment of inflammatory disorders.
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.