Background: Polycystic ovarian syndrome (PCOS) is a prevalent endocrine condition associated with hormonal and metabolic abnormalities, as well as behavioral modifications. Aim: This research assesses the impact of the chemically profiled Pluchea dioscoridis ethanolic extract and metformin in a letrozole-induced polycystic ovary syndrome rat model. Methods: Thirty female Sprague Dawley rats were allocated into five groups: Control, P. dioscoridis (100 mg/kg), PCOS (letrozole, 1 mg/kg), PCOS + Metformin (300 mg/kg), and PCOS + P. dioscoridis (100 mg/kg), letrazole was given for 8 weeks followed by metformin or P. dioscoridis for 21 days. Behavioral assessments, hormone analyses, and dopamine quantifications in the brain were performed. Ovarian histology and immunohistochemical analysis were conducted. Results: Letrozole-induced PCOS resulted in heightened depression- and anxiety-like behaviors, along with significant hormonal imbalances compared to the control group (P < 0.05%). Both P. dioscoridis and metformin therapies significantly ameliorated these changes, with P. dioscoridis demonstrating better efficacy. P. dioscoridis medication regulated luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estrogen levels, concurrently enhancing cerebral dopamine levels. Histological analysis revealed less cystic follicles and a reinstated normal ovarian architecture in rats treated with P. dioscoridis compared to PCOS group (P < 0.05%). Several flavonoids, nitrogenous compounds and hydroxy cinnamic acid esters were detected in P. dioscoridis samples for the first time utilizing UPLC-ESI-MS analysis. Conclusion: The P. dioscoridis ethanolic extract exhibited potential medicinal properties that are equivalent to or surpass those of metformin for treating behavioral, hormonal, and ovarian structural abnormalities produced by PCOS. It significantly improved dopamine levels, hormonal balance, and ovarian histology, rendering it a suitable alternative or complementary treatment for PCOS.

Background: Various techniques have been used to restore large bone abnormalities, but they have limitations. Mesenchymal stem cells (MSCs) have the potential to differentiate into bone tissue and are a promising candidate for cell therapy. Aim: This study aimed to investigate the effectiveness of using bone marrow-derived mesenchymal stem cells (MSCs) to treat femoral bone defects in rats. Material and Methods: The study was carried out in the Faculty of Medicine, Suez Canal University. The study involved dividing 27 male rats into control, defect, and stem cell-treated groups. The rats' locomotor activity, oxidative stress, inflammatory markers [tumor necrosing factor (TNF-α) and interleukin (IL-6)], angiogenic markers, osteoblast markers [Osteopontin and transforming growth factor (TGF-β)], and bone healing were assessed through various tests and measurements (histologically and radiologically). Results: The stem cell-treated group exhibited significantly improved locomotor activity, levels of inflammatory markers, total antioxidant capacity, and osteoblast markers compared to the defect group. Histological and radiological assessments indicated improvements in the stem cell-treated group. Conclusion: bone marrow-derived MSCs can enhance experimental bone healing by modulating oxidative stress, and inflammatory and angiogenic markers leading to improved locomotor parameters.

In tune with the light/dark cycle of the environment, melatonin is secreted on a circadian rhythm. After the lights go out, circulating melatonin levels gradually rise and peak in the middle of the dark phase. Herein, we studied the possible protective timing of melatonin administration on monosodium glutamate‐induced cerebellar ataxia in rat models. Thirty‐two adult albino male were randomly categorized into four groups: control group, MSG group (4 g/kg/day), day‐time melatonin group (MSG + melatonin, 10 mg/kg/day at 9.00 a.m.), and night‐time melatonin group (MSG + melatonin, 10 mg/kg/day at 9.00 p.m.). After 10 days of injections, behavioral assessments and serum melatonin were measured. Then rats were sacrificed, cerebellar immunohistopathology, oxidative stress (GPX, GR, NO, iNOS), gene expression of pro‐inflammatory genes (PI3K, TNF‐α, IL‐6) and antioxidant genes (NRF2/HO‐1) were assessed. Administration of MSG significantly caused motor deficits, increased levels of NO, INOS, PI3K, TNF‐α, and IL‐6 levels ( p < 0.05), while significantly decreased GPX, GR, NRF2/HO‐1, and serum melatonin level ( p < 0.05). Histological analysis revealed that MSG exerted degenerative effects, including the presence of pyknotic Purkinje cells, with strong positive reactions for COX2. However, melatonin administration improved these parameters in both treated groups with the superiority of the night melatonin in improving motor behaviors, histological parameters, decreasing COX2 levels, INOS, PI3K, and increasing the expression of NRF2 levels, and increasing the serum melatonin levels. Night‐time melatonin administration was more effective in protection against motor incoordination and cerebellar damage than day‐melatonin administration.