Protective Effect of Ipragliflozin on Acute Brain Injury Induced by Endotoxemia in Mice

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Mohammad A.R.; Shnaien A.A.; Alabsawy S.K.; Hassan E.S.

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Journal Paper

Paper Information

Journal: Iranian Journal of War and Public Health Year:2023 | Volume:15 | Issue:3 Page(s): 225-231

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Information Journal Paper

Title

Protective Effect of Ipragliflozin on Acute Brain Injury Induced by Endotoxemia in Mice

Author(s)

Mohammad A.R. | Shnaien A.A. | Alabsawy S.K. | Hassan E.S. | Issue Writer Certificate

Keywords

Endotoxemia

Sepsis

Tumor necrosis factor-alpha

Toll-like receptor 4

Abstract

Aims: This study was done to investigate the potential neuroprotective effect of ipragliflozin during Endotoxemia in mice. Materials & Methods: Twenty-four adult male Swiss-albino mice aged 8-12 weeks (25-35g) were randomized into four equal groups (n=6): sham (laparotomy without cecal ligation and puncture (CLP), Sepsis (laparotomy with CLP), vehicle (equivalent volume of DMSO before CLP), and ipragliflozin (3mg/kg/day, orally before CLP). Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1β, Toll-like receptor 4 (TLR4), and P-signal transducer and activator of transcription (STAT)-3 levels were assessed in the brain tissue and histological examination was done. Findings: The tissue levels of TNF-α, IL-6, and IL-1B in the sham group were much lower than in the Sepsis and vehicle groups. Furthermore, the ipragliflozin group had considerably lower tissue levels of TNF-α, IL-6, and IL-1B compared to the Sepsis and vehicle groups. However, the sham group showed much lower tissue levels of TLR4 and STAT3 compared to the Sepsis and vehicle groups. Also, the tissue levels of TLR4 and STAT3 in the ipragliflozin group were considerably lower than those in the Sepsis and vehicle groups. Histopathology analysis demonstrated that ipragliflozin might considerably reduce brain damage compared to Sepsis and vehicle groups that showed interstitial edema and included glial cells with pyknotic nuclei. Conclusion: Ipragliflozin attenuates brain dysfunction during CLP-induced polymicrobial Sepsis in male mice.

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