Abstract:In this study, the histological, immunohistochemical, morphometric, and biochemical changes to pancreatic beta-cells in STZ-induced diabetes were evaluated in rats treated with different doses of caffeine. Fifty adult male Wistar albino rats were divided into five groups: the nondiabetic control group, the diabetic untreated group, and three diabetic groups treated with different doses of caffeine (10, 50, and 100 mg/kg/day). Blood glucose and serum insulin levels were measured. The pancreata were collected and processed into paraffin sections. They were stained using hematoxylin and eosin (H&E) and Masson trichrome stains. The insulin expression in beta-cells was assessed using immunohistochemistry. Morphometrically, the percentage area of anti-insulin antibody reaction, the percentage of beta-cells per total islet cell number, and the average area of the islets were determined. STZ-induced degenerative changes in beta-cells led to decreases in the number of functioning beta-cells and insulin immunoreactivity and to increases in the number of collagen fibers in the islets. In STZ-treated rats, caffeine significantly decreased blood glucose concentration while increasing blood insulin levels at the highest applied dose. It also induced a significant increase in the number of immunoreactive beta-cells. In conclusion, caffeine may have a protective role in the biochemical and microscopic changes in pancreatic beta-cells in diabetes induced in rats through STZ administration.
Introduction. Spinal cord injury (SCI) is a life-disrupting condition in which the first few days are the most critical. Secondary conditions remain the main causes of death for people with SCI. The response of different cell types to SCI and their role at different times in the progression of secondary degeneration are not well understood. The aim of this study was to study the histopathological changes of compressed spinal cord injury (CSCI) in a rat model. Material and methods. Forty adult male Sprague-Dawley rats were divided into four groups. In group I, the rats were left without any surgical intervention (control). In group II, the rats were subjected to laminectomy without spinal cord compression (sham-operated). In group III, the rats were sacrificed one day after CSCI. In group IV, the rats were sacrificed seven days after CSCI. The light microscopy was employed to study the morphology using H&E, osmic acid staining and immunohistochemistry to detect glial fibrillary acidic protein (GFAP). The electron microscopy was applied for ultrastructure study. Results. Histopathological examination of the posterior funiculus of the white matter revealed minute hemorrhages and localized necrotic areas on day 1, which transformed to areas of cavitation and fibrinoid necrosis surrounded by a demarcating rim of numerous astrocytes by day 7. The mean percentage of area of GFAP expression increased significantly by day 7. Osmic acid staining revealed swollen nerve fibers after one day, while numerous fibers had been lost by day 7. An ultrastructure study revealed swollen redundant thinned myelin and myelin splitting, as well as degeneration of axoplasm on day 1. On day 7, layers of the myelin sheath were folded and wrinkled with partial or complete demyelination areas. The myelin lamellae were disorganized and loose. The G-ratio was significantly greater on day 1 than day 7 after CSCI. Conclusions. In the rat model of CSCI details of the progressive spinal cord injury can be analyzed by morphological methods and may be helpful in the identification of the onset and type of clinical intervention.
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