RESUMO
Introduction: Infertility may have a variety of causes that can affect both the male and female reproductive systems. Cyclophosphamide is a drug used in chemotherapy and immune system suppression. Leaf extracts of Mangifera indica exhibit a wide spectrum of pharmacological properties which have been shown in studies, including antioxidant and protective advantages. This study evaluate the antagonistic implications of leaf extracts of Mangifera indica on the testis following the exposure to cyclophosphamide. Methods: 25 male Wistar rats were assigned to five groups with five rats in each. Group A (Control), Group B (administered 150 mg of cyclophosphamide only), Group C (administered 50 mg of extracts of leaf extracts of Mangifera indica only), Group D (administered 150 mg of cyclophosphamide and 50 mg of leaf extracts of Mangifera indica) and Group E (administered 150 mg of cyclophosphamide and 100 mg of leaf extracts of Mangifera indica) for two weeks. The rats were euthanized under the anesthetic of ketamine (30 mg/kg IP). Blood was taken by cardiac puncture for biochemical examination. Testes were excised, preserved in 10% Neutral Buffered Formalin for histological investigation. One-way analysis of variance was used to examine the data, and then the Student Newman-Keul post-hoc analysis was performed. The significance of the result was assessed using p < 0.05. Results: The study showed statistically significant differences (p < 0.05) in the hormonal assay, including LH, FSH, and testosterone across all test groups, with group B (cyclophosphamide only) having significantly lower levels. Cyclophosphamide administration was observed to have a negative effect on the testicular histology and immunohistochemical results and leaf extracts of Mangifera indica attenuated the damage induced by cyclophosphamide in groups D and E. Conclusion: Leaf Extracts of Mangifera indica considerably reduced the effects of cyclophosphamide-induced changes in testis.
RESUMO
PURPOSE: Several studies have established impaired testicular function in obese male population, including the young males with childhood obesity, contributing to increased male infertility, which is a universal trend in the last few decades. Short chain fatty acids (SCFAs) have been recently demonstrated to inhibit progression to metabolic comorbidities. The present study therefore hypothesized that SCFAs, acetate attenuates testicular dysfunction in high fat diet (HFD)-induced obese rat model, possibly by modulating Nrf2/PPAR-γ. METHODS: Adult male Wistar rats weighing 160-190 g were randomly allotted into three groups (n = 6/group): The groups received vehicle (distilled water), 40% HFD and sodium acetate (200 mg/kg) plus 40% HFD respectively. The administration lasted for 12 weeks. RESULTS: HFD caused obesity, which is characterized with increased body weight and visceral adiposity and insulin resistance/hyperinsulinemia. In addition, it increased testicular lipid deposition, malondialdehyde, pro-inflammatory mediators, lactate/pyruvate ratio, γ-Glutamyl transferase, and circulating leptin as well as decreased testicular glutathione, nitric oxide, Nrf2, PPAR-γ and circulating follicle stimulating hormone and testosterone without a significant change in testicular lactate dehydrogenase, blood glucose and luteinizing hormone when compared to the control group. Nevertheless, administration of acetate reversed the HFD-induced alterations. CONCLUSION: The present results demonstrates that HFD causes obesity-driven testicular dysfunction, associated with testicular lipid deposition, oxidative stress, and inflammation. The study in addition suggests the restoration of testicular function in obese animals by acetate, an effect that is accompanied by elevated Nrf2/PPAR-γ.
RESUMO
Polycystic ovarian syndrome (PCOS), is a multifactorial endocrine disorder in women of reproductive age. It usually associates with metabolic disorders (MDs), which aggravates the risk of infertility, cardiometabolic events and associated comorbidities in women with PCOS. Adiponectin, a circulating protein produced by adipocytes, which has been suggested to inversely correlate with MDs. Spironolactone, a non-selective mineralocorticoid receptor (MR) antagonist, has been in wide clinical use for several decades. Herein, we investigated the effects of low dose spironolactone (LDS) and the role of adiponectin in endocrine-metabolic disturbances in experimentally-induced PCOS rats. Eighteen female Wistar rats (160-180 g) were randomly allotted into 3 groups and treated with vehicle (p.o.), letrozole (LET; 1 mg/kg) and LET + LDS (0.25 mg/kg), once daily for 21 days, respectively. The results showed that LET-treated animals had features of PCOS, characterized by elevated plasma testosterone and prolactin, increased body weight gain and ovarian weight as well as disrupted ovarian cytoarchitecture and degenerated follicles. Additionally, elevated fasting blood glucose, 1 h-postload glucose and plasma insulin, impaired glucose tolerance, insulin resistance, reduced insulin sensitivity, increased plasma and ovarian lipid profile, plasma lipid peroxidation, TNF-α, IL-6 and decreased plasma glutathione peroxidase and glutathione content were observed. These alterations were associated with decreased circulating adiponectin and were reversed when treated with LDS. The present results suggest that LDS ameliorates endocrine-metabolic disturbances and inflammation-related comorbidities associated with LET-induced PCOS by modulating circulating androgen-adiponectin status.
