Aubergine stem restores reproductive damages following diabetes mellitus induction in male mice.

Diabetes mellitus unbalances cellular antioxidant levels. This phenomenon can potentially lead to cellular damage and apoptosis in the male reproductive system. Besides, herbal-based antioxidants can prevent these detrimental changes. Thus, we assessed the probable role of Aubergine stems with antioxidant and anti-hyperlipidemic characteristics on reproductive damage following diabetes mellitus induction. Forty male NMRI mice were categorized into groups of control and treatments. Diabetes was induced by a single dose of streptozotocin (60 mg/kg), and the extract was administered at various doses (100, 300, and 500 mg/kg) daily for 4 weeks. Antioxidative features of the extract were approved by phytochemical assays and ferric-reducing ability of plasma. Side-effects of diabetes were also assessed by the malondialdehyde (MDA) and Griess techniques. Sperm parameters, LH, FSH, and testosterone levels, the TUNEL assay, histopathologic alteration, and apoptotic genes (p53, caspase-3, Bcl-2) were evaluated. Results showed that diabetes increased oxidation levels and the extract accelerated total antioxidant capacity status. Sperm parameters and hormone levels were restored following extract administration in diabetic animals. Also, the apoptosis rate decreased following extract administration in diabetic animals. We concluded that diabetes can elevate the levels of oxidation and suppress the antioxidant power. These pathologic changes were restored by Aubergine stem, leading to decreased levels of apoptosis and normal serum levels of testosterone, LH, and FSH.

Effects of Rosmarinus officinalis on orchitis following spermatic cord torsion-detorsion in male mice with emphasis on anti- inflammatory and antioxidant properties.

Orchitis as inflammation of testis occurs following traumatic injuries such as testicular torsion leading to high levels of oxidative stress and inflammation. Rosmarinus officinalis is a herb with anti-inflammatory and antioxidant properties. This study assessed therapeutic effects of rosemary following testicular torsion. A total of 36 male mice were categorised; control, torsion, rosemary (100 and 200 mg/kg) and torsion+rosemary groups. Torsion was induced surgically, and rosemary was gavaged. Total antioxidant capacity of extract was approved by Ferric Reducing Ability of Plasma. Malondialdehyde and Griess protocols were hired to assess oxidative stress. Finally, sperm parameters and testosterone levels were analysed. Immunofluorescent (of Tumour Necrosis Factor Alpha), hematoxylin and eosin stainings and expression of inflammatory genes (Interleukin-1α, Interleukin-1ß, Interferon-γ) were also assessed. Data were analysed using SPSS (v. 19), and graphs were drawn by GraphPad Prism (v. 9). Significantly (p < .05), oxidative stress indices and inflammatory genes expression were increased in torsion group, and total antioxidant capacity was increased in rosemary groups. In torsion+rosemary groups, total antioxidant capacity, sperm parameters and testosterone levels were increased, and inflammatory gene expression decreased significantly (p < .05). Rosemary with anti-inflammatory and antioxidant properties accelerates testicular healing in torsion cases, especially in therapeutic dose of 200 mg/kg.

Alteration of TGFB1, GDF9, and BMPR2 gene expression in preantral follicles of an estradiol valerate-induced polycystic ovary mouse model can lead to anovulation, polycystic morphology, obesity, and absence of hyperandrogenism.

OBJECTIVE: In humans, polycystic ovary syndrome (PCOS) is an androgen-dependent ovarian disorder. Aberrant gene expression in folliculogenesis can arrest the transition of preantral to antral follicles, leading to PCOS. We explored the possible role of altered gene expression in preantral follicles of estradiol valerate (EV) induced polycystic ovaries (PCO) in a mouse model. METHODS: Twenty female balb/c mice (8 weeks, 20.0±1.5 g) were grouped into control and PCO groups. PCO was induced by intramuscular EV injection. After 8 weeks, the animals were killed by cervical dislocation. Blood serum (for hormonal assessments using the enzyme-linked immunosorbent assay technique) was aspirated, and ovaries (the right ovary for histological examinations and the left for quantitative real-time polymerase) were dissected. RESULTS: Compared to the control group, the PCO group showed significantly lower values for the mean body weight, number of preantral and antral follicles, serum levels of estradiol, luteinizing hormone, testosterone, and follicle-stimulating hormone, and gene expression of TGFB1, GDF9 and BMPR2 (p<0.05). Serum progesterone levels were significantly higher in the PCO animals than in the control group (p<0.05). No significant between-group differences (p>0.05) were found in BMP6 or BMP15 expression. CONCLUSION: In animals with EV-induced PCO, the preantral follicles did not develop into antral follicles. In this mouse model, the gene expression of TGFB1, GDF9, and BMPR2 was lower in preantral follicles, which is probably related to the pathologic conditions of PCO. Hypoandrogenism was also detected in this EV-induced murine PCO model.

Genetic, biochemical and histopathological evaluations of thymoquinone on male reproduction system damaged by paclitaxel in Wistar rats.

This study was aimed to evaluate therapeutic effects of thymoquinone on male reproductive damages induced by paclitaxel. Forty-eight male rats were divided; control, paclitaxel (4 mg/kg), paclitaxel + thymoquinone (1.25, 2.5 and 5 mg/kg) and thymoquinone (1.25, 2.5 and 5 mg/kg). Paclitaxel and thymoquinone were administrated intraperitoneally for 4 and 14 days respectively. Then, the testes were removed for H&E staining, sperm parameters and apoptotic genes expression assessments. Serum levels of nitric oxide, total antioxidant capacity and testosterone were evaluated, and sperm DNA fragmentation was assessed. Paclitaxel significantly (p < .05) increased nitric oxide, decreased total antioxidant capacity and reduced testosterone levels than control group. Sperm motility, viability and count were significantly (p < .05) reduced in paclitaxel group than control. Co-administration of thymoquinone + paclitaxel caused decreased levels of nitric oxide and increased total antioxidant capacity, testosterone levels and reproductive parameters than paclitaxel group significantly (p < .05). Paclitaxel significantly (p < .05) increased caspase-3 and p-53 and decreased Bcl-2 genes expression than control. Sperm DNA fragmentation index was also increased significantly (p < .05) in paclitaxel group than control, and this value was decreased in whole doses of paclitaxel + thymoquinone groups than paclitaxel. Thymoquinone can alleviate the side effects of paclitaxel on the male reproductive system.