The current study was designed to investigate the protective role of diosmin against cyclophosphamide-induced premature ovarian insufficiency (POI). Female Swiss albino rats received a single intraperitoneal dose of cyclophosphamide (200 mg/kg) followed by 8 mg/kg/day for the next 15 consecutive days either alone or in combination with oral diosmin at 50 or 100 mg/kg. Histopathological examination of ovarian tissues, hormonal assays for follicle stimulating hormone (FSH), estradiol (E2), and anti-Mullerian hormone (AMH), assessment of the oxidative stress status, as well as measurement of the relative expression of miRNA-145 and its target genes [vascular endothelial growth factor B (VEGF-B) and regulator of cell cycle (RGC32)] were performed. Diosmin treatment ameliorated the levels of E2, AMH, and oxidative stress markers. Additionally, both low and high diosmin doses significantly reduced the histopathological alterations and nearly preserved the normal ovarian reserve. MiRNA-145 expression was upregulated after treatment with diosmin high dose. miRNA-145 target genes were over-expressed after both low and high diosmin administration. Based on our findings, diosmin has a dose-dependent protective effect against cyclophosphamide-induced ovarian toxicity in rats.

Reaching a postmortem diagnosis of hypothermia is challenging in forensic practice. Therefore, this study was conducted to detect the histopathological, histochemical and biochemical changes that occur in adult albino rats following exposure to induced fatal hypothermia. Twenty-four adult albino rats were divided into the negative control, moderate hypothermia, severe hypothermia and hypoxia groups. Rats in the control group were euthanized when those in the moderate hypothermic group died. Blood samples were collected via heart puncture, and the cerebrum, heart, suprarenal gland, kidney, liver and skeletal muscle were removed to investigate the biochemical, histochemical and histopathological changes. Postmortem assessment depicted significant changes in lipid peroxidation, represented by increased malondialdehyde levels in the studied organs of the rats in hypothermic and hypoxia groups. Histopathological examination of the rats' organs revealed degeneration and necrosis in the hypothermia and hypoxia groups. Sections taken from the severe hypothermic rats revealed a loss of normal cardiac tissue architecture, necrotic changes in the pyramidal cells in the cerebral cortex, and massive necrosis, mainly in the tubules of the renal cortex and medulla. These findings suggest that histological changes might be used as biochemical markers for postmortem diagnosing of fatal hypothermia, particularly in severe hypothermic conditions. KEY POINTS• Death by hypothermia is a serious public health problem worldwide.• Confirming a diagnosis and determining the cause of death in cases of hypothermia are among the most difficult practices in forensic medicine. • Death by hypothermia might be associated with structural abnormalities in various organs. • Studies using different tissue staining techniques will enable an overall illustration of the role of histopathological changes in body organs as indicators of hypothermia.

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Methotrexate (MTX) is a folic acid antagonist, widely used as a chemotherapeutic and immunosuppressive drug, but it is toxic to reproductive systems. In recent years, the era of stem cell applications becomes a promising point as a possible therapeutic agent in male infertility. This study is aimed at evaluating the therapeutic effects of stem cells at histological, molecular, biochemical, and functional levels in a methotrexate-induced testicular damage model. Material and Methods. Thirty rats were divided randomly into three groups (ten rats each): group 1 (control): animals received an intraperitoneal injection of 2 ml phosphate-buffered saline per week for 4 weeks, group 2 (MTX-treated group): animals were intraperitoneally injected with methotrexate (8 mg/kg) once weekly for 4 weeks, and group 3 (ADMSC-treated group): methotrexate-treated animals received a single dose of 1 × 10 6 stem cells/rat at the 5th week. At the 8th week, blood samples were collected for hormonal analysis; then, animals were sacrificed. The testes were dissected; the right testis was stained with hematoxylin and eosin. Random sections were taken from group 3 and examined with a fluorescent microscope. The left testis was divided into two specimens: the first was used for an electron microscope and the second was homogenized for molecular and biochemical assessments. Results. Group 2 showed significant histological changes, decreased free testosterone level, decrease in stem cell factor expression, and dysfunction of the oxidation state. The results revealed significant improvement of these parameters. Conclusion. Transplantation of adipose tissue-derived stem cells (ADMSCs) can improve the testicular damage histologically and functionally in a rat model.

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