Partial recovery from alloxan-induced diabetes by sodium phthalhydrazide in rats

Publication date: November 2017
Source:Biomedicine & Pharmacotherapy, Volume 95
Author(s): Irina G. Danilova, Tatyana S. Bulavintceva, Irina F. Gette, Svetlana Yu Medvedeva, Victor V. Emelyanov, Musa T. Abidov
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.



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