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Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis

  • Authors:
    • Çiğdem Sevim
    • Mustafa Ozkaraca
    • Mehtap Kara
    • Ali Taghizadehghalehjoughi
    • Sidika Genç
    • Yesim Yeni
    • Ali Sefa Mendil
    • Marios Spanakis
    • Eren Ozcagli
    • Sergey V. Kuzmin
    • Demetrios A. Spandidos
    • Aristides Tsatsakis
  • View Affiliations / Copyright

    Affiliations: Department of Medical Pharmacology, Faculty of Medicine, Kastamonu University, 37200 Kastamonu, Türkiye, Department of Pathology, Faculty of Veterinary, Cumhuriyet University, 58070 Sivas, Türkiye, Department of Pharmaceutical Toxicology, Faculty of Pharmacy, Istanbul University, 34116 Istanbul, Türkiye, Department of Medical Pharmacology, Faculty of Medicine, Bilecik Seyh Edebali University, 11230 Bilecik, Türkiye, Department of Medical Pharmacology, Faculty of Medicine, Turgut Ozal University, 44210 Malatya, Türkiye, Department of Pathology, Faculty of Veterinary, Erciyes University, 38280 Kayseri, Türkiye, Department of Forensic Sciences and Toxicology, Faculty of Medicine, University of Crete, 71003 Heraklion, Greece, Federal Budgetary Establishment of Science ‘F.F. Erisman Scientific Centre of Hygiene’, Federal Service for Surveillance on Consumer Rights Protection and Human Wellbeing (Rospotrebnadzor), Mytishchi, Moscow 141014, Russian Federation, Department of Virology, Faculty of Medicine, University of Crete, Heraklion 71003, Greece
    Copyright: © Sevim et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 52
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    Published online on: December 13, 2024
       https://doi.org/10.3892/mmr.2024.13417
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Abstract

The 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‑α, 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.
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Copy and paste a formatted citation
Spandidos Publications style
Sevim Ç, Ozkaraca M, Kara M, Taghizadehghalehjoughi A, Genç S, Yeni Y, Mendil AS, Spanakis M, Ozcagli E, Kuzmin SV, Kuzmin SV, et al: Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis. Mol Med Rep 31: 52, 2025.
APA
Sevim, Ç., Ozkaraca, M., Kara, M., Taghizadehghalehjoughi, A., Genç, S., Yeni, Y. ... Tsatsakis, A. (2025). Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis. Molecular Medicine Reports, 31, 52. https://doi.org/10.3892/mmr.2024.13417
MLA
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."Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis". Molecular Medicine Reports 31.2 (2025): 52.
Chicago
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."Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis". Molecular Medicine Reports 31, no. 2 (2025): 52. https://doi.org/10.3892/mmr.2024.13417
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Spandidos Publications style
Sevim Ç, Ozkaraca M, Kara M, Taghizadehghalehjoughi A, Genç S, Yeni Y, Mendil AS, Spanakis M, Ozcagli E, Kuzmin SV, Kuzmin SV, et al: Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis. Mol Med Rep 31: 52, 2025.
APA
Sevim, Ç., Ozkaraca, M., Kara, M., Taghizadehghalehjoughi, A., Genç, S., Yeni, Y. ... Tsatsakis, A. (2025). Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis. Molecular Medicine Reports, 31, 52. https://doi.org/10.3892/mmr.2024.13417
MLA
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."Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis". Molecular Medicine Reports 31.2 (2025): 52.
Chicago
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."Exploring the anti‑inflammatory activity of boron compounds through the miR‑21/PTEN/AKT pathway in cecal ligation and puncture‑induced sepsis". Molecular Medicine Reports 31, no. 2 (2025): 52. https://doi.org/10.3892/mmr.2024.13417
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