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<p>Hypertensive nephropathy (HTNeph), primarily triggered by vascular endothelial dysfunction, is the second most common cause of end-stage renal disease. This study investigates the ameliorative effect of dulaglutide, a glucagon-like peptide-1 receptor agonist, on HTNeph via its impact on renal vascular endothelial growth factor (VEGF) and peroxisome proliferator-activated receptors-gamma (PPARγ). The effect of dulaglutide (0.2 mg/kg/day, s.c.) for six weeks on L-NAME-induced hypertension (50 mg/kg/day, i.p.) was investigated in rats. Renal function biomarkers, serum IL-10 and TNF-α, tissue redox balance, histopathological and immunohistochemical changes, and PPARγ gene expression were assessed. Coadministration of dulaglutide with L-NAME could recover renal glomerular and vascular histological structure, reduce collagen deposition, increase the anti-inflammatory IL-10 and the reno-protective PPARγ level, elevate the immunohistochemical expression of the renal tubular eNOS and VEGF, and substantially reduce TNF-α activity in hypertensive rats. Our research linked dulaglutide’s anti-inflammatory, antifibrotic, antioxidant, and vascular endothelium-promoting qualities to its capacity to upregulate VEGF and PPARγ, which confer its reno-protective effects. Thus, dulaglutide is presented as a potential candidate to shield patients from HTNeph.</p><p></p>

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Renoprotective effect of dulaglutide in L-NAME-induced hypertensive nephropathy in rats: insight into the roles of PPAR-gamma and VEGF

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月28日

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  • Nermeen Bastawy,
  • Aliaa E. M. K. El-Mosallamy,
  • Rabab Ahmed Rasheed,
  • A. S. Sadek,
  • R. T. Khattab,
  • Esraa Ali,
  • Randa A. Zaghloul,
  • Wael B. A. Ghaly,
  • Amy F. Boushra

摘要

Hypertensive nephropathy (HTNeph), primarily triggered by vascular endothelial dysfunction, is the second most common cause of end-stage renal disease. This study investigates the ameliorative effect of dulaglutide, a glucagon-like peptide-1 receptor agonist, on HTNeph via its impact on renal vascular endothelial growth factor (VEGF) and peroxisome proliferator-activated receptors-gamma (PPARγ). The effect of dulaglutide (0.2 mg/kg/day, s.c.) for six weeks on L-NAME-induced hypertension (50 mg/kg/day, i.p.) was investigated in rats. Renal function biomarkers, serum IL-10 and TNF-α, tissue redox balance, histopathological and immunohistochemical changes, and PPARγ gene expression were assessed. Coadministration of dulaglutide with L-NAME could recover renal glomerular and vascular histological structure, reduce collagen deposition, increase the anti-inflammatory IL-10 and the reno-protective PPARγ level, elevate the immunohistochemical expression of the renal tubular eNOS and VEGF, and substantially reduce TNF-α activity in hypertensive rats. Our research linked dulaglutide’s anti-inflammatory, antifibrotic, antioxidant, and vascular endothelium-promoting qualities to its capacity to upregulate VEGF and PPARγ, which confer its reno-protective effects. Thus, dulaglutide is presented as a potential candidate to shield patients from HTNeph.