Abstract
Otostegia persica extract was used as a traditional medicine for the management of diabetes mellitus in humans in some parts of Iran. This study investigated the effects of O. persica oral extract on pancreatic beta cells in streptozotocin-induced diabetic rats by stereological methods. Thirty-two matured normoglycemic male Sprague–Dawley rats, weighing 180–220 g, were selected and randomly divided into four groups: Control group consists of normal rats which did not receive the extract during the study. Diabetic group comprises diabetic rats but did not receive any extract. Treated control group rats were normal but received the extract at a dose of 500 mg/kg/day. Treated diabetic group (TD) was made up of diabetic rats and received the extract (500 mg/kg/day). Diabetes was induced by a single intraperitoneal injection of 50 mg/kg of streptozotocin. After 1 month, all the rats received deep anesthesia with ether, and then, the pancreas was dissected and processed. Isotropic uniform and random sections were obtained by orientator method. Volume of pancreatic beta cells and also volume density of pancreatic island were studied, using stereologic and ultrastereological methods. Blood glucose level (BGL) and blood insulin level (BIL) were measured in different phases during the investigation. Statistical analysis by one-way analysis of variance test showed the presence of hypertrophic changes in the volume of the remaining beta cells in diabetic group, not in the controls. But such changes reduced significantly (P < 0.05) in the TD group which received the extract. Also, a significant reduction in pancreatic islet volume in diabetic and TD groups was seen, in comparison with the controls (P < 0.01). BGL decreased significantly in TD group, compared to the diabetic group (P < 0.001). BIL decreased in diabetic and TD groups in comparison to the controls (P < 0.05). This study demonstrated that O. persica oral extract can play an effective role in the management of diabetes and probably by controlling the hyperglycemic condition and not stimulating the beta cell to increase insulin secretion can help prevent to a large extent the entering of the remaining beta cells to some pathologic changes, like hypertrophy.
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