ArticleBMC pharmacology & toxicology2026
Tranexamic acid inhibits mitochondrial DNA release and reduces inflammatory response in an in vitro model of OGD/R-induced Caco-2 cell injury.
Article in BMC pharmacology & toxicology, 2026. 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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Abstract
backgroundIschemia-reperfusion (I/R) injury of the intestine remains a challenging clinical issue, and there is currently no definitive treatment protocol. Tranexamic acid (TXA), an antifibrinolytic drug used in bleeding patients, has been shown in previous studies to protect the intestinal epithelial barrier, but the specific mechanism remains unclear. This study aimed to explore the molecular mechanisms by which TXA protects the intestinal barrier after intestinal I/R.
methodsThe cell viability assay was assessed to verify the cytotoxicity of TXA toward Caco-2 cells. A Caco-2 cell oxygen-glucose deprivation-reperfusion (OGD/R) model was established. The transepithelial electrical resistance (TEER) of Caco-2 cell monolayers and FITC-dextran permeability assays were performed to assess the intestinal barrier function. The JC-1 fluorescent probe was used for assessment of mitochondrial membrane potential. Quantitative PCR (qPCR) was used to quantify mitochondrial DNA (mtDNA) released by Caco-2 cells, and enzyme-linked immunosorbent assay (ELISA) was employed to assess inflammatory factors.
resultsTXA reversed OGD/R-induced decreases in TEER and increases in FITC-dextran permeability in Caco-2 cell monolayers. Microscopy images of the Caco-2 monolayer also support these results. Additionally, TXA enhanced mitochondrial membrane potential, suppressed mtDNA release and alleviated inflammatory responses.
conclusionsTXA protects the intestinal barrier after intestinal I/R by enhancing mitochondrial membrane potential, inhibiting mtDNA release and reducing inflammation, suggesting its potential as a therapeutic agent for intestinal I/R injury.
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