Figure - available from: Histochemistry and Cell Biology
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Primordial follicles surrounded by single-layer flat follicle cells can be seen in the ovarian cortex from the sham group. The oocyte in the center of the primordial follicle and the surrounding flat-shaped follicular cells are normal in appearance (a). The zona pellucida is preserved in a Graafian follicle, although the granulosa cells surrounding the oocyte are discontinuous. The interna and externa layers of the theca follicle are well developed (b). Theca and granulosa lutein cells in the structure of the corpus luteum can be easily distinguished. The blood vessels around them are surrounded by a regular endothelium, and their lumen is open (c, d). Lymph capillaries and numerous blood vessels can be seen in the loose connective tissue of the medulla (e). There are numerous hilus cells, thought to be analogs of Leydig cells (f). OE ovarian epithelium, TE theca follicle, GC granulosa cells, CR corona radiata, ZP zona pellucida, O oocyte, GLC granulosa lutein cells, TLC theca lutein cells, V blood vein, M medulla, HC hilus cells, Lv lymph vessel. Bars: (a, d) 10 μm, (b) 40 μm, (c, e, f) 20 μm
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This study aimed to investigate the effects of curcumin treatment on ovaries at different periods of the diabetes disease. Fifty-six female Wistar albino rats (250–300 g) aged 12 weeks were divided into seven groups. No treatment was applied to the control group. The sham group was given 5 mL/kg of corn oil, and the curcumin group 30 mg/kg curcumin...
Citations
... The latter reflects either dysfunctional pancreatic beta cells with a marked decrease in insulin synthesis or a resistance of the peripheral insulin-dependent systems to insulin activity, in both cases inducing chronic hyperglycemia. If left untreated, this persistently high blood glucose will affect the function of major organs such as the heart, blood vessels, nerves, eyes, and kidneys contributing to poor quality of life (Tufekci and Kaplan 2022). ...
Diabetes mellitus is a chronic metabolic disease characterized by persistent hyperglycemia, revealing a decrease in insulin efficiency. The sustained glucotoxic pancreatic microenvironment increases reactive oxygen species generation, resulting in chronic oxidative stress responsible for massive DNA damage. This triggers PARP-1 activation with both NAD⁺ and ATP depletion, affecting drastically pancreatic beta cells’ energy storage and leading to their dysfunction and death. The aim of the present study is to highlight the main histological changes observed in pancreatic islets pre-treated with a unique NADH intraperitoneal injection in a streptozotocin-(STZ)-induced diabetes model. In order to adjust NADH doses, a preliminary study with three different doses, 500 mg/kg, 300 mg/kg, and 150 mg/kg, respectively, was conducted. Subsequently, and on the basis of the results of the aforementioned study, Wistar rats were randomly divided into four groups: non-diabetic control group, diabetics (STZ 45 mg/kg), NADH-treated group (150 mg/kg) 15 min before STZ administration, and NADH-treated group (150 mg/kg) 15 min after STZ administration. The effect of NADH was assessed by blood glucose level, TUNEL staining, histo-morphological analysis, and immunohistochemistry. The optimum protective dose of NADH was 150 mg/kg. NADH effectively decreased hyperglycemia and reduced diabetes induced by STZ. Histologically, NADH pre-treatment revealed a decrease in beta cell death favoring apoptosis over necrosis and therefore preventing inflammation with further beta cell destruction. Our data clearly demonstrate that NADH prior or post-treatment could effectively prevent the deleterious loss of beta cell mass in STZ-induced diabetes in rats and preserve the normal pancreatic islet’s function.
Graphical abstract
