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Effect of black tea on histological and immunohistochemical changes in pancreatic tissues of normal and streptozotocin‐induced diabetic mice (Mus musculus)
Authors:Ramar Manikandan  Ramalingam Sundaram  Raman Thiagarajan  Mullaivanam Ramasamy Sivakumar  Velayutham Meiyalagan  Munusamy Arumugam
Affiliation:1. Centre for Animal Health and Management, Alagappa University, Karaikudi, Tamil Nadu, India;2. Department of Zoology, University of Madras, Chennai, Tamil Nadu, India
Abstract:The aim of the present study is to evaluate the effect of hot water extract of black tea in regenerating β 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 β cells. The dose of streptozotocin not only altered the function of β 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 β cells when stained with chrome hematoxylin and phloxine. Interestingly, pancreatic sections of diabetic mice fed with black‐tea extract showed regeneration of β cells and acinar region appeared normal with increased numbers of β 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 β cells by its antioxidant action against nitrosative stress in streptozotocin‐induced diabetes. Microsc. Res. Tech., 2009. © 2009 Wiley‐Liss, Inc.
Keywords:black tea  pancreas  streptozotocin  diabetes  nitric oxide synthase
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