Evidence map›Paper›PMID 42157803›Full record

ArticleIranian journal of pharmaceutical research : IJPR

Probiotics Ameliorate Atrial Fibrillation-Associated Biomarkers and Inflammation in Rats via Modulation of the Gut Microbiota and NLRP3 Inflammasome Pathway.

Yeran Zhu, Long Bai, Ruibin Li, Yichen Li, Hongxia Hou, Jidong Zhang

Abstract read
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Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yeran ZhuAffiliated Hospital of Hebei University, Baoding, China.
Long BaiThe Second Hospital of Hebei Medical University, Shijiazhuang, China.
Ruibin LiThe Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yichen LiThe Second Hospital of Hebei Medical University, Shijiazhuang, China.
Hongxia HouAffiliated Hospital of Hebei University, Baoding, China.
Jidong ZhangThe Second Hospital of Hebei Medical University, Shijiazhuang, China.ORCID https://orcid.org/0009-0003-0100-8290

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The gut-heart axis, particularly the role of gut microbiota and the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, is increasingly implicated in the pathogenesis of atrial fibrillation (AF). While probiotics show therapeutic potential, their mechanism in AF remains unclear. Objectives: This study investigates whether probiotics mitigate AF pathology by restoring gut microbiota homeostasis and inhibiting NLRP3 activation. Methods: An AF model was induced in rats via acetylcholine (ACH)/CaCl₂ infusion. Animals were divided into five groups: Sham, AF, AF+Probiotics, AF+MCC950 (NLRP3 inhibitor), and AF+Probiotics+MCC950. We analyzed gut microbiota (16S rRNA sequencing), serum short-chain fatty acids (SCFAs; GC-MS), and the expression of NLRP3 pathway components [NLRP3, caspase-1, interleukin-1β (IL-1β)] and AF biomarkers [pentraxin 3 (PTX3), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), chemerin, galectin-3 (Gal-3)] via immunohistochemistry (IHC), Western blot, and real-time quantitative polymerase chain reaction (RT-qPCR). Results: Atrial fibrillation rats exhibited gut dysbiosis, characterized by reduced diversity (Shannon index significantly decreased vs. Sham, P < 0.01), decreased beneficial bacteria (e.g., Lactobacillus), and lower SCFA levels (acetic, propionic, and butyric acids reduced by 40 - 50%, P < 0.05). Probiotics restored microbial diversity, increased SCFA production (to levels comparable to Sham, P < 0.05), and suppressed NLRP3 inflammasome activation, as evidenced by reduced levels of NLRP3, caspase-1, and IL-1β (protein and mRNA expression decreased by 50 - 70%, P < 0.01). Consequently, the expression of key AF biomarkers was significantly downregulated (PTX3, IL-6, TNF-α, chemerin, Gal-3 reduced by 40 - 60%, P < 0.05). The combined intervention of probiotics and MCC950 yielded the most pronounced effects (all markers further reduced vs. either treatment alone, P < 0.05). Conclusions: Probiotics alleviate AF-related inflammation and biomarker expression, potentially by modulating the gut microbiota and inhibiting the NLRP3 inflammasome pathway. These findings highlight the gut-heart axis as a promising target for AF management.

Indexed as

Atrial FibrillationIntestinal MicrobiotaNLRP3 Inflammasome Signaling PathwayProbiotics

Identifiers

PMID42157803
PMCPMC13181812

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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.