Nephrotoxicity is one of the limiting factors for using doxorubicin (DOX). Interleukin 1 has major role in DOX-induced nephrotoxicity, so we investigated the effect of interleukin 1 receptor antagonist diacerein (DIA) on DOX-induced nephrotoxicity. DIA (25 and 50 mg/kg/day) was administered orally to rats for 15 days, in the presence or absence of nephrotoxicity induced by a single intraperitoneal injection of DOX (15 mg/kg) at the 11th day. We measured levels of serum urea, creatinine, renal reduced glutathione (GSH), malondialdehyde (MDA), total nitrites (NOx), catalase, and superoxide dismutase (SOD). In addition, caspase-3, tumor necrosis factor alpha (TNFα), nuclear factor kappa B (NFκB) expressions, and renal histopathology were assessed. Our results showed that DOX-induced nephrotoxicity was ameliorated or reduced by both doses of DIA, but diacerein high dose (DHD) showed more improvement than diacerein low dose (DLD). This protective effect was manifested by significant improvement in all measured parameters compared to DOX treated group by using DHD. DLD showed significant improvement of creatinine, MDA, NOx, GSH, histopathology, and immunohistochemical parameters compared to DOX treated group.

Background: Insulin dependent diabetes mellitus is a chronic metabolic disease. Many drugs used in its treatment which have a number of serious adverse effects. Natural agent as quercetin (QCT) has been suggested in the alternative medicine for treatment of diabetes mellitus. Aim of the work:To evaluate the effect of QCT on the histological changes which occur in the islet of Langerhans of the streptozotocin (STZ)-induced diabetic rats and the possible mechanisms through which QCT produces its protective effect. Materials and methods:Fourty five male albino rats were divided into 3 groups: Group I, control group; 15 rats received single intraperitoneal injection of citrate buffer saline. Group II, diabetic group; 15 rats received single intraperitoneal injection of STZ. Group III; QCT-treated group, 15 rats received daily intraperitoneal injections of QCT for 30 days prior to, and for 30 days after the single injection of STZ. Blood samples were taken for monitoring blood glucose levels. Pancreas was taken out and processed for light microscopic, immunocytochemical and morphometrical studies.Results: Blood glucose levels showed a significant increase in group II compared to the control, while a significant decrease was observed in groups III compared to group II (all p<0.05). In the hematoxylin-eosin stained sections, STZ administration caused marked degeneration of islet Beta cells with inflammatory cells infiltration. Using QCT; in group III, reversed most of the pancreatic morphological changes, and interestingly some islets noticed with connections to some pancreatic ducts. In chrome alum heamatoxylin stained sections, STZ administration caused a significant decrease in the number of bluish stained β cells compared to controls. While group III showed a significant increase in β cells number compared to group II (all p<0.05). Sections of animals injected with charcoal, showed many charcoal labeled macrophages in group II compared to group III, and controls. There was increased iNOS and caspase 3 immunoreactivity in islets cells of group II than in controls, and was decreased in group III. Conclusion:This study provides evidence that quercetin could exert a protective effect against β cell damage by its anti-inflammatory, anti-apoptotic, and antioxidant effects; and aids regeneration of β cells which might through stimulation of the ductal stem cells. However, further experimental studies are still needed for more details on quercetin as an adjuvant drug in management of diabetes mellitus. Journal of Diabetes and MetabolismCitation: Rifaai RA, El-Tahawy NF, Saber EA, Ahmed R (2012) Effect of Quercetin on the Endocrine Pancreas of the Experimentally Induced Diabetes in Male Albino Rats: A Histological and Immunohistochemical Study. J Diabetes Metab 3:182.

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Introduction: Diabetes mellitus is a global problem and several restoration approaches have been developed to induce beta (β) cells regeneration. Platelet rich plasma (PRP) is an autogenous and economical source of growth factors which nowadays used in the tissue repair. Aim:To test the hypothesis that PRP could play a role in the improvement of the structural changes occurred in the endocrine pancreas of experimentally-induced diabetic rats and the possible mechanisms through which PRP induced its effects to shed a light on the possible use of such application in the clinical field. Material and methods:Sixty male albino rats were used; 20 for obtaining the PRP and 40 were divided into 4 equal groups (10 rats each): control, PRP-group, diabetic group, PRP/diabetic group. Diabetes was induced by single intra-peritoneal injection of streptozotocin (50-60 mg/kg). The PRP was administered by SC injections in a dose of 0.5 mg/kg twice weekly for 3 weeks. Results:The diabetic group showed a significant increase in blood glucose levels compared to the control. Treatment with PRP significantly reduced the blood glucose levels compared to the diabetic group. The diabetic group showed variable marked morphological changes which diminished by the PRP administration. PRP/diabetic group had a significant increase in the mean number of pancreatic islets and β-cells/islet compared to the diabetic group. The islet cells appeared normal with scarcely seen vacuolations. The duct system showed several changes; stratifications, invagination of the surface epithelium to the underlying connective tissue, and sprouting of the ductal epithelial cells in between the lobules. Numerous small islets were noticed in a close association with the intralobular ducts. Small newly lobules with abundant connective tissue were organized. There were significant increases in the insulin immunopositive β-cells and PCNA positive cells in PRP/diabetic group compared to diabetic group. Conclusion:This study provides an evidence of the diabetic pancreatic islet regeneration in response to PRP treatment. The PRP stimulated islet cell regeneration and stimulated the induction of other sources of β-cells generation as the exocrine portion of the pancreas; ductal and acinar cells. In addition, PRP might put the pancreas into an environment similar to the postnatal developmental one where new lobules were formed. These will pave the future for a novel treatment for diabetes.

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Tramadol is a synthetic, centrally acting analgesic. It is the most consumed narcotic drug that is prescribed in the world. Tramadol abuse has dramatically increased in Egypt. Long term use of tramadol can induce endocrinopathy. So, the aim of this study was to analyze the adrenal insufficiency induced by long term use of tramadol in experimental animals and also to assess its withdrawal effects through histopathological and biochemical genetic study. Forty male albino rats were used in this study. The rats were divided into 4 groups (control group, tramadol-treated group, and withdrawal groups). Tramadol was given to albino rats at a dose of 80 mg/kg body weight for 3 months and after withdrawal periods (7–15 days) rats were sacrificed. Long term use of tramadol induced severe histopathological changes in adrenal glands. Tramadol decreased the levels of serum cortisol and DHEAS hormones. In addition, it increased the level of adrenal MDA and decreased the genetic expression of glutathione peroxidase and thioredoxin reductase in adrenal gland tissues. All these changes started to return to normal after withdrawal of tramadol. Thus, it was confirmed that long term use of tramadol can induce severe adrenal insufficiency.

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Sepsis is a leading cause of death among intensive care patients. During sepsis, exaggerated reaction to infection leads to massive production of reactive oxygen species and inflammatory mediators, which eventually leads to multiple organ damage. Silymarin is a well-known antioxidant and cytoprotective agent, which showed protective effects in different models of disease. Thus, we hypothesized that silymarin would be protective against sepsis-induced liver and kidney injury. Sepsis was induced in rats by the cecal ligation and puncture (CLP) method. Rats were divided into sham, CLP-non-treated and CLP treated with silymarin (100 mg/kg, i.p. 1 h following CLP). After 24 h, rats were euthanized for blood and tissue samples, which were used for assessment of MDA, NO, GSH, IL-6 and TNF-α levels and SOD activity, in addition to renal and hepatic function parameters. Survival study was conducted using another set of animals following the same previously mentioned procedure. Silymarin showed protective effects evidenced by enhanced overall survival following sepsis (80% in silymarin-treated vs. 20% in septic group), in addition to improvement of hepatic and renal function parameters and reduction of MDA, NO, IL-6 and TNF-α levels. Moreover, silymarin supported the endogenous antioxidant mechanisms via elevation of GSH levels and reinforcement of SOD activity. In conclusion, silymarin protects against sepsis-induced hepatic and renal injury, possibly via antioxidant and anti-inflammatory mechanisms.