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Kseniia Sokolova,

Kseniia Sokolova,

Ural Federal University, Russian Federation

Title: Regeneration and apoptosis of β-cells in Lanhergance islets at experimental diabetes mellitus type 2 and at it correction by sodium phthalhydrazide in rats


Biography: Kseniia Sokolova,


Introduction: Diabetes mellitus type 2 (DM2) is always accompanied by inflammation and destruction of β-cells. Cytokines, secreted by macrophages, are the main mediators of inflammatory and regenerative processes. In previous studies we demonstrated partial recovery of functional activity of β-cells at the injections of sodium phthalhydrazide, which changes macrophage phenotype M1→M2 and reduce inflammation.

Objective: The main objective of this study is the peculiarities of islet β-cells regeneration at DM2 and at modulation activity of macrophages.

Materials & Methods: Twenty (20) Wistar adult rats were divided into four groups: one –control; two and three – 30 and 60 days of streptozotocin/nicotinamide-induced diabetes correspondingly; four – 30 days of diabetes + injections of sodium phthalhydrazide. White blood parameters were evaluated on a hemoanalyzer. Cytokines were measured in blood and pancreas using ELISA method. Insulin+, KI67+cells were detected by immunohistochemistry. Detection of DNA fragmentation in apoptotic cells was made by TUNEL method kits.

Results: The results indicated that at the experimental diabetes quantity of white blood cells (WBC), lymphocytes and pro-inflammatory cytokines TNFα and Ifnγ in blood significantly increases. Concentration of anti-inflammatory TGFβ decreases both in blood and in pancreas. Sodium phthalhydrazide reduces quantity of WBC and lymphocytes and concentration of Ifnγ in blood and level of TNFα in pancreas. At 30th day of diabetes quantity of apoptotic β-cells increases and Ki67+β-cells are appeared. At sodium phthalhydrazide, quantity of Ki67+ β-cells increases significantly, while the quantity of apoptotic cells decreases. General and local inflammation at diabetes leads to the destructive-degenerative processes in pancreas, while modulation activity of macrophages, which reduces inflammation, intensifies islet regeneration.