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Article citations


M. Okumura, M. Imanishi, M. Okamura, M. Hosoi, N. Okada, Y. Konishi, T. Morikawa, K. Miura, T. Nakatani and S. Fujii, “Role for Thromboxane A2 from Glomerular Thrombi in Nephropathy with Type 2 Diabetic Rats,” Life Sciences, Vol. 72, No. 24, 2003, pp. 2695-2705. doi:10.1016/S0024-3205(03)00180-2

has been cited by the following article:

  • TITLE: Effect of Cyclooxygenase-2 Blockade on Renal Hypertrophy Development during Early Diabetes Mellitus

    AUTHORS: Beatriz Vázquez-Cruz, Josseline Rangel-Veladiz, David Segura-Cobos, Pedro López-Sánchez, Maximiliano Ibarra-Barajas, Dante Amato

    KEYWORDS: COX-2; Prostaglandins; TGF-β; Diabetic Nephropathy; Renal Hypertrophy; Angiotensin II

    JOURNAL NAME: Pharmacology & Pharmacy, Vol.4 No.3, May 31, 2013

    ABSTRACT: Diabetes mellitus is the leading cause of diabetic nephropathy; the early phase of diabetes is associated with kidney growth and hyperfiltration; several factors modulate these changes, among them, prostaglandins and angiotensin II. Previous studies have shown that cyclooxygenase-2 is implicated in experimental models of diabetes. The aim of this work was to study the effect of celecoxib treatment on renal hypertrophy development in early diabetes mellitus. In our rats with early streptozotocin-induced diabetes there was renal hypertrophy, and increased renal expression of cyclooxygenase-2, AT1 receptor, and transforming growth factor-β1. Treatment with the selective cyclooxygenase-2 inhibitor celecoxib reduced the urinary excretion of prostaglandins such as prostaglandin E2, 6-keto prostaglandin F1α, and thromboxane B2. Kidney hypertrophy was reversed by the treatment, and the renal expression of cyclooxygenase-2, AT1 receptor, and transforming growth factor-β1 decreased. The renoprotective effects of celecoxib were independent of the changes in plasma glucose levels. These results confirm that cyclooxygenase-2 inhibition in rats with streptozotocin-induced diabetes decrease renal hypertrophy; this effect in turn, may be mediated by reduction of the expression of AT1 receptors and transforming growth factor-b1 in the kidney.