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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., (Copyright © 2010 Wiley-Liss, Inc.)

The aim of this study is to evaluate the effect of curcumin in protecting against selenium-induced toxicity in liver and kidney of Wistar rats. Light microscopy evaluation of selenium alone administered rats showed liver to be infiltrated with mononuclear cells, vacuolation, necrosis, and pronounced degeneration. Control liver sections showed a regular morphology of parenchymal cells with intact hepatocytes and sinusoids. Kidney from selenium alone administered rats showed vacuolar degeneration changes in the epithelial cells, cellular proliferation with fibrosis, thickening of capillary walls, and glomerular tuft atrophy. Such changes were also observed in rats administered with selenium and curcumin simultaneously and rats administered first with selenium and then curcumin 24 h later. Interestingly, such degenerative changes observed in liver and kidney induced by selenium were not seen in rats that were administered with curcumin first and selenium 24 h later. This clearly suggests the protective nature of curcumin against selenium toxicity. To understand the probable mechanism of action of curcumin, we analyzed inducible nitric oxide synthase (iNOS) expression by immunohistochemistry, and the results showed an increased iNOS expression in selenium-alone induced liver and kidney. Such high iNOS levels were inhibited in liver and kidney of rats pretreated with curcumin and then with selenium 24 h later. Based on the histological results, it can be concluded that curcumin functions as a protective agent against selenium-induced toxicity in liver as well as kidney, and this action is probably by the regulatory role of curcumin on iNOS expression., ((c) 2009 Wiley-Liss, Inc.)

The aim of the present study is to evaluate the effect of hot water extract of black tea in regenerating beta cells in streptozotocin-induced diabetic mice. Light microscopic examination of pancreatic sections of streptozotocin-induced diabetic mice showed the acinar cells to be small, shrunken, and with deteriorated beta cells. The dose of streptozotocin not only altered the function of beta cells but also damaged the acinar region. The changes in acinar cells were coarsening of endoplasmic reticulation suggesting alteration in their secretory function. The control pancreatic tissue showed well-defined granulated islets and dark beta cells when stained with chrome hematoxylin and phloxine. Interestingly, pancreatic sections of diabetic mice fed with black-tea extract showed regeneration of beta cells and acinar region appeared normal with increased numbers of beta cells. To understand the probable mechanism of action of black-tea extract, we analyzed inducible nitric oxide synthase (iNOS) expression by immunohistochemistry and the results showed an increased iNOS levels in streptozotocin-induced diabetic pancreas, and such high iNOS levels were inhibited in black-tea extract treated mice. According to histological results obtained, it can be concluded that the black-tea extract helps in regeneration of damaged pancreas and protects pancreatic beta cells by its antioxidant action against nitrosative stress in streptozotocin-induced diabetes.