The aim of this study is to investigate the mechanism of an action of compound isolated from Vitex negundo in
streptozotocin-induced diabetic mice. Light microscopic examination of liver, kidney and pancreatic sections of
streptozotocin-induced diabetic mice showed changes like coarsening of acinar cells of endoplasmic reticulum, destruction of β-cells, and alteration in their secretory function were observed in the pancreas. Changes like dilation of vein, unusual concentric arrangement of hepatocytes, and
liver fibrosis were observed in the liver. Thickening of tubules and expansion of glomerulus were observed in kidneys. All these altered parameters were reversed close to normal condition upon treatment using
idopyranose. The results show the
antidiabetic potential of
idopyranose. Interestingly, liver, kidney, and pancreatic sections of diabetic mice fed with the isolated 1, 2 di-substituted
idopyranose showed regeneration of hepatocytes, nephrocytes, as well as β-cells and acinar region appeared normal with increased numbers of β-cells. To understand the probable mechanism of action of 1, 2 di-substituted
idopyranose, we analyzed proinflammatory
inducible nitric oxide synthase (iNOS) and
nuclear factor-kappa B (NF-κB) expression by immunohistochemistry and the results showed an increased iNOS and NF-κB levels in
streptozotocin-induced diabetic liver, kidney and pancreas. Such high iNOS and NF-κB levels were inhibited in 1, 2 di-substituted
idopyranose treated mice. The results suggest that 1, 2 di-substituted
idopyranose helps in the protection of hepatocytes, nephrocytes and pancreatic β-cells probably by its action against NF-κB and iNOS mediated
inflammation in
streptozotocin-induced diabetes.