Sevim, Ç.Ozkaraca, M.Kara, M.Taghizadehghalehjoughi, A.Genç, S.Yeni, Y.Mendil, A.S.Spanakis, M.Ozcagli, E.Kuzmin, S.V.Spandidos, D.A.Tsatsakis, A.2025-01-122025-01-122025.01.011791-2997https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=dspace_ku&SrcAuth=WosAPI&KeyUT=WOS:001382082800001&DestLinkType=FullRecord&DestApp=WOS_CPLhttps://hdl.handle.net/20.500.12597/33927The present study investigated the impact of boric acid (BA) and borax (BX) on markers of inflammation and modifications in miR-21/PTEN/AKT pathway genes in the liver and kidney tissues of Sprague Dawley male rats with sepsis induced by cecal ligation and puncture (CLP). A total of 60 male Sprague Dawley rats were randomly divided into 6 groups, each containing 10 animals as follows: Control, CLP (where the model was created), 20 mg/kg BX (CLP + BX1), 40 mg/kg BX (CLP + BX2), 20 mg/kg BA (CLP + BA1) and 40 mg/kg BA (CLP + BA2). Liver and kidney tissues were analyzed for histopathological changes, immunopositivity for tumor necrosis factor-alpha, interleukin (IL)-6 and IL-10, and gene expression of microRNA-21 (miR-21), phosphatase and tensin homolog (PTEN) and AKT. Gene expression analysis in the liver tissues revealed a significant decrease in miR-21, and a marked but not significant decrease in PTEN levels in the CLP group, while AKT expression was significantly increased in the CLP group, and was significantly decreased in CLP + BA1 group compared with in the CLP group. In the kidney tissues, miR-21 levels were significantly decreased in the CLP group, but the CLP + BA2 group showed a significant increase compared with in the CLP group. These results suggest the potential therapeutic benefits of low-dose BA and BX in ameliorating sepsis-induced tissue damage, emphasizing the need for further exploration of their mechanisms of action.eninfo:eu-repo/semantics/openAccessboraxboric acidcytokinesepsisseptic shockCLP-modelExploring the anti-inflammatory activity of boron compounds through the miR-21/PTEN/AKT pathway in cecal ligation and puncture-induced sepsisArticle10.3892/mmr.2024.134170013820828000013121791-3004