Several studies highlight beneficial effect of glabridin as an anti-hyperglycemic agent. However, the protective mechanisms of glabridin on improvement of pancreatic islets damage due to streptozotocin (STZ) exposure have not been adequately investigated. In the present study, we aimed to elucidate the effects of glabridin on restoration of pancreatic islet architecture, at least in part by restoring collagen I and fibronectin, through an activation of protein kinase Cs (PKCs) and transforming growth factor (TGF)-β1 in STZ-induced pancreatic β-cell injuries. Glabridin (40 mg/kg b.wt./day) was administrated to STZ-exposed rats for 8 weeks. The effects of glabridin were then investigated by measuring body weight, blood glucose level, pancreatic morphology, and protein expressions of PKCs, TGF-β1, collagen I, and fibronectin. The results revealed that glabridin prevented weight loss and significantly decreased blood glucose level. Physical distortion and impairment with irregular outline was clearly observed in untreated STZ islets. Nevertheless, rat islets showed nearly normal architecture with a high β-cell number after glabridin treatment. Glabridin also ameliorated the expression levels of PKCs, TGF-β1, collagen I, and fibronectin in STZ-rat pancreas. These results provide novel evidence that glabridin significantly reduced pancreatic islets abnormalities in STZ-exposed rats and these effects could be associated with its hypoglycemic activity and with restoration of normal levels of PKCs, TGF-β1, collagen I and fibronectin, which could subsequently contribute to maintaining islet structure and function.
Key words: Glabridin, pancreas, diabetes mellitus, anti-hyperglycemia, anti-oxidant activity, streptozotocin.
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