Curcumin induces regeneration of β cells and suppression of phosphorylated-NF-κB in streptozotocin-induced diabetic mice

Objectives: This study aimed to assess the immunomodulatory effect of curcumin on innate and adaptive immune responses, as well as its inhibitory power on hyperglycemia in streptozotocin (STZ)-induced diabetic CD1 mice. Material and methods: Mice were divided into six groups as follows: normal control mice (I), mice were intraperitoneally (i.p.) injected with either citrate (II), DEMSO (III), or curcumin (170 mg/kg, 3 times/week, for 28 days) (IV), as well as a single intraperitoneal injection of STZ (160 mg/kg) (V) and STZ mice treated with curcumin (VI). The anti-diabetic effect was assessed by estimation of the blood glucose concentration on days 3, 10, 17, 24, and 31. Differential count of white blood cells and the levels of cytokines were also measured at all previous time points. Pancreatic islets were examined for histopathological changes, and the immunohistochemical analysis for insulin and phosphorylated-nuclear factor-kappa B (phospho-NF-kappa B) was done at the end of the study. Results: After curcumin administration, hyperglycemia was improved compared to diabetic mice; however, glucose concentration remains above the normal level. Treatment with curcumin selectively increased the count of lymphocytes and monocytes but decreased the granulocyte count in STZ diabetic mice. Diabetic mice treated with curcumin showed lower levels of interferon (IFN)-gamma, interleukin (IL)-6, and IL-1 beta, as well as a higher level of IL-2 than in diabetic mice. Histopathological alterations that accompanied diabetes induction were ameliorated after curcumin administration. The pancreatic islets of treated diabetic mice displayed a decline in the immunostaining positivity of phospho-NF-kappa B compared to diabetic mice. Conclusion: These results suggest that curcumin has anti-diabetic properties as it can improve the damage caused to the pancreatic beta cells by its preferential immunomodulatory action on T helper1-related cytokines, as well as the immunosuppressive activity on proinflammatory cytokines.