ArticleMolecular biology reports2024
The hepatoprotective effect of sodium butyrate on hepatic inflammatory injury mediated by the NLRP3 inflammatory pathway in subchronic fluoride-exposed mice.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Effects of Sodium Butyrate on Digestive Metabolism, Blood Gas Parameters and Blood Biochemical Indices in Tumbler Pigeons Based on Untargeted Metabolomics.Animals : an open access journal from MDPI · 2026Article
- Potential mechanisms by which microbiota-accessible carbohydrates regulate hepatic lipid metabolism in MAFLD via the gut-liver axis.Frontiers in microbiology · 2026Review
- Exploring the Mechanism of Bu Zhong Yi Qi Decoction in Treating Sepsis-induced Acute Lung Injury based on Network Pharmacology and Experimental Verification.Current pharmaceutical design · 2026Article
- Sodium butyrate attenuates sodium fluoride-induced cardiac injury in rats via modulating oxidative stress, inflammation, and apoptosis.Scientific reports · 2025Article
- Curcumin suppresses NLRP3 inflammasome activation by inducing autophagy to alleviate neuropathic pain in rats.Molecular biology reports · 2025Article
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11 authors.
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Abstract
backgroundExcessive subchronic fluoride exposure can cause severe damage to detoxification organs, including the liver. Sodium butyrate has anti-inflammatory, antitumor, antioxidant and immunomodulatory properties. However, relatively few studies have investigated the effects of sodium butyrate on liver injury caused by subchronic fluoride exposure. The purpose of this research was to investigate the effect and mechanism of sodium butyrate on fluoride-induced hepatic inflammatory injury via the expression of nod-like receptor protein 3 (NLRP3).
methodsMice were subjected to randomization into four groups, control group (C), fluorosis group (F), sodium butyrate alone group (S), and treatment group (Y). The mice in groups F and F + S drank 100 mg/L sodium fluoride-containing distilled water freely every day. After fluoride exposure lasted for 3 months, the mice in group S and F + S were gavaged with sodium butyrate daily at a concentration of 1000 mg/kg. Following the treatment regimen, liver specimens were collected for analysis. The mRNA and protein expression levels of inflammatory factors and NLRP3 and its downstream gene were measured by RT-qPCR and western blotting.
resultsThe histological hematoxylin and eosin (H&E) staining of liver showed that the subchronic fluoride-exposed group were chronic inflammation. The liver of treatment group were less vacuolar degeneration and inflammatory infiltration. The results of the biochemical assay showed that the subchronic fluoride-exposed group were liver injury. In addition, the detection of oxidative stress indicators showed that chronic subchronic fluoride exposure could lead to an increase in the level of oxidative stress in the liver, and the treatment alleviated this increase. RT-qPCR results showed that compared with those in the control group, the mRNA levels of the inflammatory factors TNF-α, IL-6 and IL-1β, the NLRP3 inflammasome and its downstream factors NLRP3, caspase-1, gasdermin D (GSDMD) and IL-18 increased in the liver tissue of mice in the subchronic fluoride-exposed group. Sodium butyrate released inflammatory factors during subchronic fluoride exposure and inhibited the protein expression of activated NLRP3 to a certain extent.
conclusionsSodium butyrate may play a protective role by antagonizing the production of activated inflammasomes and their downstream inflammatory factors in the livers of subchronic fluoride-exposed mice.
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