Effect of Carbenoxolone on Inflammatory Cytokine Levels, Fasting Blood Sugar, and Histopathology of Pancreas on Experimental Autoimmune Diabetes in C57BL/6 Mice

Background and Destruction of insulin-producing beta cells by T cells causes type-1 diabetes (T1D). Carbenoxolone has cytoprotective and anti-inflammatory effects, and has been shown to be capable of suppressing Th17 cells that are effectively involved in the pathogenesis of type 1 diabetes, therefore, we studied the effect of Carbenoxolone on T1D in C57BL/6 mice.
Forty male C57BL/6 inbred strain mice were randomly divided into four groups and in three groups diabetes was induced by streptozotocin. A positive control group was considered and two other groups received 50 mg/kg/day i.p. carbenoxolone (7 and 5 doses). Then, on days 7 and 14 after the disease induction, fasting blood sugar (FBS) level, anti-inflammatory cytokines IL-1β, IL-6 and TNF-α, and pathological changes of the pancreas were studied during the course of the disease.
Carbenoxolone increased the levels of IL-1β, IL-6, TNF-α, and FBS. Also, it significantly increased infiltration of inflammatory cells into the pancreatic islets (P It seems that carbenoxolone triggers a breakdown in Treg/Th17 balance by increasing the levels of pro-inflammatory cytokines and increases the number of Th17 cells, thereby causing toxic effects on the pancreatic beta cells and increasing the severity of the disease.