ArticleJournal of inflammation research2025
Protective Effects of Irisin Against LPS-Induced Intestinal Injury and Its Influence on Gut Microbiota in Septic Mice.
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.
What it found
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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.
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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.
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Who cites it
1 citing paper in PubMed.
- Gut barrier-microbiota crosstalk in sepsis: from pathogenesis to potential therapies.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Irisin, a novel myokine, has garnered significant attention for its roles in metabolic regulation and anti-inflammatory responses. Sepsis disrupts the intestinal microenvironment, exacerbating its progression and highlighting the need for novel therapeutic approaches. This study aims to investigate whether irisin exerts protective effects against lipopolysaccharide (LPS)-induced intestinal injury in septic conditions and to explore the underlying mechanisms involving the gut microbiota. Methods: To induce sepsis, C57BL/6 mice were injected intraperitoneally with LPS at a dose of 10 mg/kg, and then administered with 1 µg/kg of irisin. The Activity levels and 7-day survival rate were recorded. The intestinal expression of irisin/FNDC5 was assessed using Western blotting and immunofluorescence staining. Inflammatory factors were measured using enzyme-linked immunosorbent assay (ELISA). Peripheral blood bacteria were cultured on blood agar plates. Intestinal histomorphology was analyzed via hematoxylin and eosin (H&E) staining. The expression of occludin and apoptotic-related proteins was determined by Western blot, and apoptotic cells were detected using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method. The intestinal microbiota was analyzed through 16S rRNA amplicon sequencing. Results: Irisin improved the survival state and rate of LPS-induced septic mice. It restored endogenous irisin/FNDC5 levels in intestinal tissues, mitigated intestinal barrier injury, and alleviated bacteremia following sepsis treatment. Furthermore, irisin exhibited anti-inflammatory properties by increasing the levels of IL-22 while decreasing those of TNF-α and IL-6, as well as anti-apoptotic effects by increasing levels of pro-caspase-3 and Bcl-2 while decreasing cleaved caspase-3, Bax, and the positive density of apoptotic cells. Additionally, it regulated intestinal microbiota dysfunction. Conclusion: Irisin effectively treats septic acute intestinal injury by reducing apoptosis and inflammation, with the intestinal microbiota likely playing a crucial role. This finding offers a novel approach to clinical management of sepsis.
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