Normal gonadal function can be disrupted by hypothyroidism. Hypothyroidism disturbs testicular function directly and centrally by affecting the hypothalamic‐pituitary‐testicular axis with unclear mechanism. As nesfatin‐1 neurons co‐localized with TRH and GnRH neurons in the hypothalamus, it could play a role in centrally hypothyroidism induced testicular dysfunction. Selenium (Se), by affecting thyroid iodide supply, could relieve these disturbances. So, we aim to identify the role of nesfatin‐1 as a link between testicular dysfunction and hypothyroidism through modulating the MAPK/ERK pathway while discussing the possible role of Se in alleviating hypothyroidism and associated testicular damage. Forty male rats were divided equally into: Control: distilled water, Se: Se orally, Propylthiouracil (PTU): PTU orally, PTU + Se: Se with PTU orally. Serum thyroid function, gonadal hormones, nesfatin‐1, testicular redox status, sperm analysis, brain tissue GnRH, nucleobindin 2‐derived polypeptide, pMAPK/ERK gene expression, histological changes and immunohistochemical expression of testicular proliferating cell antigen (PCNA) were done. PTU induced hypothyroidism and reduction of gonadal hormones which both were correlated with reduced nesfatin‐1. There was testicular stress with reduced GnRH, NUCB2, pMAPK/ERK gene expression, and PCNA immunopositive cells. These parameters were reversed by Se. Nesfatin‐1 could be the central link between hypothyroidism and disturbances of the hypothalamic pituitary testicular axis.

Background: Cisplatin is frequently used as an anticancer medication. Nephrotoxicity and hepatotoxicity are triggered by its usage, causing patients to limit their long-term therapy. Aim: To investigate the underlying mechanism of omega-3 (fatty acids) effect on hepatorenal toxicity induced by cisplatin in rats and to detect whether it has a protective or therapeutic effect or both and the role of HO-1 enzyme in both effects. Materials and Methods: 40 male rats were divided into four equal groups: Control group: received i.p. saline+ corn oil orally, Cisplatin Group: received i.p. CP (12 mg/kg)+ corn oil orally, Cisplatin+ ω-3 pretreatment group: received i.p. CP following 10 days of ω-3 pretreatment in dose {(270 mg/kg) EPA, (180 mg/kg)} and Cisplatin+ ω-3 post-treatment group: received i.p. CP followed by 10 days of ω-3 post-treatment in dose as the previous group. Liver and kidney function, serum (HO-1), serum& tissue (TNF-α, IL-10), tissue (NFkB, GSH, MDA), and NrF2 gene expressions were measured. Results: Cisplatin-induced marked hepatorenal failure; detected by elevation of serum: AST, ALT, creatinine, and urea. Also, serum& tissue (TNF-α, IL-10), and tissue (NFkB, GSH, MDA) were significantly changed with no change in NrF2 gene expressions as compared to the control. On other hand, pre or post-ω-3 intake significantly corrected the changed markers. Liver and renal histopathological and immunohistochemical changes confirmed the biochemical results in all groups. Conclusion: Cisplatin treatment impairs liver and kidney function, while ω-3 supplementation could avoid this toxicity, with the protective response appearing to be more beneficial than the therapeutic effect.

Aims: This study aims to investigate the role of gut microbiota in polycystic ovarian syndrome (PCOS) induction by monosodium glutamate (MSG) with the study of the protective effect of flaxseeds. Methods: 24 female rats were divided into three groups: Group 1: distilled water; Group 2: MSG; and Group 3: flaxseed + MSG. Finally, body and ovarian weights, HOMA-IR, plasma (gonadal hormones, triglycerides, HDL, LDL, adiponectin, TNF-α, IL-6, and lipopolysaccharides), intestinal (alkaline phosphatase, myeloperoxidase, Trimethylamine N-oxide, and free fatty acid receptor 2 gene expression), ovarian tissue (Silent Information Regulator 1 (SIRT1), reduced glutathione, and gene expression of mitogen activated protein kinase (AMPKα) and SIRT1) were determined. In addition, vaginal swaps, ovarian histopathology, and immunohistochemical staining of BCL2 and Bax were done. Results: MSG-induced insulin resistance, dyslipidemia, intestinal dysbiosis, ovarian oxidative stress, and inflammation through modulation of the AMPKα/SIRT1 pathway. On the other hand, flaxseed significantly prevented these findings. Conclusion: MSG-induced gut dysbiosis that predisposes to PCOS and ingestion of flaxseed can be considered a prospective protective agent against PCOS development.