Abstract

The main reason for the development of type 1 diabetes is decrease of the absolute number of B‐cells and their functional activity. The goal of our study was to investigate the regulation of B‐cells regeneration and function.The model of alloxan diabetes was simulated on male Wistar rats according the author's modified method. The treatment of animals responded EC Directive 2010/63/EU. The content of macrophages was determined by the immunohistochemical study of the pancreatic sections (MAC387) (Abcam), and the number of proliferating B cells was detected with double immunohistochemical staining (insulin antibodies (clone E11D7, Millipore) and Ki67 (BD)). The number and size of pancreatic islets were counted. The derivatives of aminoftalhydrozide were used as the modulators of macrophage activity (patent). The density of B‐cells, their proliferative and secretory activity were significantly decreased of the pancreas of diabetic animals, the average size of islets was also decreased. The number of macrophages in the pancreas islets of diabetic animals was drastically increased. This was reduced by half after immunomodulation. The result of immunomodulation was the increase of islets' size, B‐cells' content and their secretory activity. Consequently, a significant decrease of glucose and Hb1c concentration and an increase of the level of insulin were observed in blood.These results afford to use the modulation of macrophage as a promising strategy in the stimulation of reparative processes in the pancreas.

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