ArticleHistology and histopathology2026
Electroacupuncture preconditioning attenuates acute lung injury in mice through transient receptor potential vanilloid 4-mediated anti-inflammation via inhibiting the p38 MAPK signaling pathway.
Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- TRPV4 drives macrophage pyroptosis via mitochondrial dysfunction and mtROS-dependent NLRP3 inflammasome activation in acute lung injury.Redox biology · 2026Article
- Review
- Acupuncture at Zusanli (ST36) for the benefits of sepsis-laboratory evidence for "preventive treatment of disease" and "holistic concept" in the protective effects of acupuncture: a literature review of rodent studies.Frontiers in neurology · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
The objective of this study was to investigate the protective effect of electroacupuncture (EA) preconditioning on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The changes in inflammatory factors and total protein content in bronchoalveolar lavage fluid (BALF) were quantified using enzyme-linked immunosorbent assay (ELISA) and bicinchoninic acid assay (BCA). Hematoxylin and eosin (H&E) staining was employed to assess the extent of lung injury, while Ly-6G immunohistochemistry was used to examine the infiltration of inflammatory cells. Western blot analysis was employed to detect the expression of TRPV4 and proteins associated with the mitogen-activated protein kinase (MAPK) signaling pathway. In comparison with the sham-operated group, the model group demonstrated an elevated production of inflammatory factors in the BALF, augmented total protein content, elevated lung injury score, increased number of Ly-6G-positive cells, upregulation of TRPV4 expression in the lung, and enhanced p38 phosphorylation. The aforementioned pathological changes were significantly improved by EA preconditioning. Furthermore, the protective effect of EA preconditioning on ALI mice was verified by the use of GSK1016790A, an agonist of TRPV4, which demonstrated that this effect is exerted through the TRPV4-mediated p38 MAPK signaling pathway.
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Registered trials
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