ArticleBMC veterinary research2026
Echinatin attenuates LPS-induced mastitis by suppressing IL-17RA and MAPK/NF-κB signaling.
Article in BMC veterinary research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundMastitis severely impairs milk yield and quality, as well as the health and productivity of dairy animals. Although antibiotics are the primary therapeutic option, their associated side effects drive the search for safer alternatives from botanical sources. Echinatin (Ech), a natural chalcone with known anti-inflammatory properties, has not been evaluated for its efficacy against mastitis. This study aimed to investigate the anti-inflammatory effects and underlying mechanisms of Ech using lipopolysaccharide (LPS)-induced bovine mammary epithelial cells (BMECs) and a mouse mastitis model.
resultsThe results demonstrated that Ech exhibited an anti-inflammatory effect by reducing the levels of inflammatory factors (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and IL-17A) and decreasing protein levels of inflammatory mediators (cyclooxygenase-2 (COX2), and inducible nitric oxide synthase (iNOS)) in vitro and in vivo. Mechanistically, RNA-seq analysis identified an association with the IL-17 A receptor (IL-17RA) signaling following Ech intervention, which was subsequently validated by western blot showing that Ech suppressed the activation of both IL-17RA and the downstream MAPK/NF-κB pathways. Furthermore, in a recombine IL-17A (rIL-17A)-induced inflammatory model in BMECs, Ech attenuated the exacerbated inflammatory response by restraining IL-17RA and the downstream MAPK/NF-κB activation. Importantly, blocking IL-17RA signaling abolished the anti-inflammatory and pathway-inhibitory effects of Ech. Collectively, these results demonstrate a vital role of IL-17RA and MAPK/NF-κB pathway for Ech-mediated protection against mammary gland inflammation.
conclusionsOur findings reveal that Ech attenuates LPS‑induced inflammation in BMECs and a mouse model of mastitis by suppressing IL-17RA signaling and thereby inactivating the MAPK/NF-κB pathway, offering new insights for optimizing preventive strategies against mastitis in dairy cows.
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.