ArticleScientific reports2025
Sodium butyrate attenuates sodium fluoride-induced cardiac injury in rats via modulating oxidative stress, inflammation, and apoptosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Terminalia arjuna Bark Nanosuspension Attenuates Fluoride-Induced Cardiotoxicity in Rats by Modulating Oxidative Stress, Inflammation and ACE Expression.Biological trace element research · 2026Article
- Gut-derived metabolites and mitochondrial homeostasis in heart failure: mechanistic links and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Enhancement of intestinal barrier function and alleviation of mycophenolic acid toxicity by a probiotic-conditioned mediumFrontiers in nutrition · 2026Article
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13 authors.
Funding
Abstract
As a well-recognized double-edged element in health and disease, low concentrations of fluoride are beneficial for preventing dental caries, but chronic exposure to excessive fluoride induces multi-system toxicity, including cardiotoxicity, for which no specific therapeutic agents are currently available. This study explored whether sodium butyrate (NaB), a natural derivative of short-chain fatty acids, attenuates sodium fluoride (NaF)-induced cardiac injury in rats by regulating oxidative stress, inflammation, and apoptosis. Forty-eight Sprague-Dawley rats were randomized into Control, NaB, NaF, and NaF + NaB groups. After 17 weeks of NaF exposure (NaB co-administered in the last 4 weeks), cardiac injury was assessed via histopathology, myocardial biomarkers, and molecular assays for oxidative stress, inflammation, and apoptosis. NaF exposure reduced the heart-to-brain weight ratio by 17.8%, dysregulated biomarkers (cTnI ↓19.3%, LDH ↑20.5%), induced histopathological damage, and disrupted oxidative stress (MDA ↑21.5%, SOD ↓19.2%, CAT ↓26.1%), inflammation (TNF-α ↑40.1%, IL-6 ↑27.9%, IL-10 ↓21.9%), and apoptosis (cleaved Caspase-3/pro-Caspase-3 ratio ↑51.1%, Bcl-2/Bax ratio ↓53.5%). NaB reversed these changes, restoring myocardial structure and molecular homeostasis. These findings indicate that NaB alleviates NaF-induced cardiac injury through antioxidant, anti-inflammatory, and anti-apoptotic effects, suggesting it may serve as a potential natural therapeutic agent for fluoride-associated cardiac injury.
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