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Sotagliflozin prevents acute kidney injury by suppressing oxidative stress, inflammation, and apoptosis in renal ischemia/reperfusion rat model
Summary
This study found that sotagliflozin, a dual SGLT1/2 inhibitor, protects against acute kidney injury in rats by reducing oxidative stress, inflammation, and cell death in a renal ischemia/reperfusion model. While not directly about microplastics, the study is relevant to understanding kidney protection mechanisms, as microplastics have been detected in kidney tissue and may contribute to renal inflammation.
Introduction and aim. Acute kidney injury (AKI) is a life-threatening condition with limited effective pharmacological options. Although sodium-glucose cotransporter 2 (SGLT2) inhibitors have shown renal protective effects, the potential role of the dual SGLT1/2 inhibitor sotagliflozin in ischemia/reperfusion injury (IRI) has not been previously investigated. We aimed to evaluate its nephroprotective properties in a rat model of renal IRI. Material and methods. Twenty-four male Sprague-Dawley rats were randomized into four groups (sham, control, dimethyl sulfoxide [DMSO], sotagliflozin). Renal IRI was induced by 40 min ischemia followed by 2 h reperfusion. Rats received either DMSO or sotagliflozin (10 mg/kg, intraperitoneally) 24 h and 1 h before surgery. Kidney function (urea, creatinine, neutrophil gelatinase-associated lipocalin [NGAL]), oxidative stress (8-iso-prostaglandin F2α [8-iso-PGF2α]), inflammation (tumor necrosis factor-alpha [TNF-α]), apoptosis (caspase-3), and histopathology were assessed. Results. In the control group, serum urea (106.5±2.9 mg/dL), creatinine (1.52±0.09 mg/dL), and NGAL (64.5±3.6 ng/mL) were significantly higher than in the sham group (32.6±5.3, 0.89±0.06, 49.5±3.8, respectively; p<0.0001). Tissue 8-iso-PGF2α (63.8±5.9 pg/mL), TNF-α (186±7 pg/mL), and caspase 3 (120.3±6.5 pmol/L) were also elevated vs. sham (35.6±3.6, 137±7, 92.3±4.9; p<0.0001). Sotagliflozin pretreatment reduced urea (53.8±2.8 mg/dL), creatinine (1.04±0.07 mg/dL), NGAL (49.6±6.4 ng/mL), 8-iso-PGF2α (41.3±3.9 pg/mL), TNF-α (140±6.6 pg/mL), and caspase 3 (89.7±2.4 pmol/L; all p<0.0001 vs. control). Histological injury scores improved from 4.0 in control to 1.0 in the sotagliflozin group (p<0.05). Conclusion. Sotagliflozin significantly improved renal function and histopathological damage in rats with renal IRI by attenuating oxidative stress, inflammation, and apoptosis. These findings support its potential as a candidate for further investigation in the prevention of AKI.
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