Partial recovery from alloxan-induced diabetes by sodium phthalhydrazide in rats - 14/11/17
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Abstract |
In the commonly used experimental model of diabetes, a cytotoxic glucose analogue alloxan can selectively destruct pancreatic β-cells, with characteristics similar to the type-1 diabetes (T1D) in humans. Treatment of diabetic rats with sodium phthalhydrazide partially reversed diabetogenic pathology in the alloxan-induced diabetes. The alloxan-treated rats with permanent hyperglycemia, which further received i.p. twenty daily doses 2mg/kg b.w. phthalhydrazide, showed at 60days of the experiment a significant amelioration of the diabetes status. Hyperglycemia was decreased by 52%, glycated haemoglobin HbA1c returned to control value, insulin concentration significantly increased from 45,4% (alloxan group) to 59,5% (alloxan+phthalhydrazide) of the control values. Importantly, phthalhydrazide treatment of alloxan-treated diabetic rats markedly decreased the concentrationof interleukin-6 (IL-6) and corticosterone level. Morphometric analysis revealed a marked increase in the number of pancreatic islets/mm2, and a number of cells/mm2 in the pancreatic islets. These changes, including 3-fold increase in the number of insulin-producing cells and 2-fold decrease in blood glucose levels, correlated with the increased proliferative activity of pancreatic β-cells in the diabetic phthalhydrazide-treated animals. Interestingly, the number of CD68+ cells/macrophages in the pancreatic islets, which was relatively high in the alloxan group (63,9+− 16.4/mm2), markedly decreased after the phthalhydrazide treatment (23,6+−7,2/mm2). Taking together with the previous data on the phthalhydrazide-related macrophage silencing, restriction of macrophage quantity in the alloxan-affected pancreatic islets can be possibly one of important events leading to the partial recovery from the β-cell disruption.
Le texte complet de cet article est disponible en PDF.Abbreviations : ADM, ATP, DAB, DNA, EGF, ELISA, GLUT2, GSH, HbA1c, IGF-1, IL-6, INF-γ, LPS, NOD, PDL, ROS, SEM, T1D, T2D, TGF, Th lymphocyte, TNF-α
Keywords : Type 1 diabetes, Alloxan-induced diabetes, Pancreatic β-cell, Heterocyclic N-hydrazides, Luminol derivative, Phthalhydrazide
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Vol 95
P. 103-110 - novembre 2017 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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