miR-25-3p ameliorates SAE by targeting the TLR4/NLRP3 axis
Open accessAbstract
Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis. It has been reported that miR-25-3p is closely related to the development of sepsis. However, the detailed mechanism of miR-25-3p in SAE requires further investigation. Caecum ligation and puncture (CLP) was performed to induce SAE in vivo. LPS stimulation was applied to mimic the in vitro inflammatory model. The expression levels of TLR4 and NLRP3 in the cerebral cortex were evaluated by immunofluorescence. The gene and protein expression levels were determined by qRT-PCR and a western blot analysis. ELISA was used to detect the levels of inflammatory cytokines. The interaction between miR-25-3p and TLR4 was validated by a dual luciferase reporter assay. TLR4 and NLRP3 were highly expressed in the cerebral cortex of SAE mice, while miR-25-3p was expressed at low levels. Activation of the inflammasome, increased release of cytokines and microglial activation were also observed in the SAE mouse model. The overexpression of miR-25-3p inhibited the expression of LPS-induced cytokines and microglial activation. Furthermore, miR-25-3p inhibited TLR4 expression by directly targeting TLR4. The anti-inflammatory effect of miR-25-3p in LPS-induced CHME5 was reversed by TLR4 overexpression. miR-25-3p overexpression attenuated the activation of microglia in SAE by inhibiting the NLRP3/IL-1β/IL-18 axis by directly targeting TLR4, suggesting that miR-25-3p may be a potential target for SAE diagnosis and treatment.
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miR-25-3p inhibits IL-1β signaling via the TLR4/NLRP3 axis.
“miR-25-3p inhibits IL-1β signaling via the TLR4/NLRP3 axis [23]”
From Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy (2026) · cites this paper as [23]
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Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy
Tan, H., Su, W., & Niu, Z. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27125390 · Cited by 1 · see citing works
“…stage: 1 ⃝ Preclinical research: CD137L neutralizing antibody TKS-1 inhibits M1 polarization [21]; α 7nAChR agonist remimazolam activates the Nrf2/HO-1 pathway [22]; miR-25-3p inhibits IL-1 β signaling via the TLR4/NLRP3 axis [23]; miR-494 maintains mitochondrial metabolic homeostasis [24].”
- Authors
- Luo, X.-Y., Ying, J.-H., & Wang, Q.-S.
- Affiliations
- University of South China (CN)
- ORCID
- Wang, Qiao-Sheng
- Venue
- Metabolic Brain Disease
- Published
- 2022-06-15
- Volume
- 37
- Issue
- 6
- Pages
- 1803-1813
- ISSN
- 0885-7490 (ISSN-L)
- 1573-7365
- PMC
- PMC9198415
- OpenAlex
- W4282937782
- Cited by
- 24
- References
- 33
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 7 · 2023: 5 · 2022: 1
- FWCI
- 1.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Metabolic Brain Disease (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- miR-25-3p, sepsis-associated encephalopathy, TLR4, NLRP3 inflammasome, microglial activation, IL-1β, IL-18, LPS-induced neuroinflammation, cerebral cortex, sepsis, microRNA therapeutic target
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Lipopolysaccharides, Cytokines, Sepsis, MicroRNAs, Toll-Like Receptor 4, Mice, Sepsis-Associated Encephalopathy
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