Background Ginseng is a powerful phytoestrogen with high antioxidant properties. Objective This study aimed to evaluate the effect of Panax Ginseng (PG) on folliculogenesis, proliferation, and apoptosis in the ovary impaired by nicotine. Methods Forty adult mice were divided into five groups. Control, sham, and nicotine groups, and co-treated groups of nicotine and ginseng in doses of 0.5 and 1 g/kg. Folliculogenesis was assessed via histopathology and serum evaluation of estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) by ELISA. Lipid peroxidation and antioxidant enzyme activities both in homogenate tissue and serum were assayed by colorimetric analysis. Apoptotic markers of cytochrome c (Cyt c), Bax, and Bcl-2 were evaluated by RT-PCR. Proliferative index was studied by the Ki-67 immunostaining procedure. Results In comparison to the control or sham groups, nicotine significantly reduced the levels of FSH, LH, and estradiol hormones. An insignificant reduction was observed in the progesterone hormone. Nicotine reduced all healthy follicle numbers, except primordial (P = 0.001). Malondialdehyde (MDA) was increased in tissue and serum in the nicotine group (P = 0.01). Serum catalase (CAT) and enzymatic activity of superoxide dismutase (SOD) both were reduced in tissue and the serum, in the nicotine group. Nicotine induced a reduction in the proliferative indexes of granulosa and theca cells in pre-antral and antral follicles (P = 0.001). However, its effect on the proliferative index of stroma cells was not significant. Apoptotic markers were elevated in the nicotine group (P = 0.001). Co-treatment with ginseng elevated all sex hormones, increased healthy follicles, and reduced tissue or serum lipid peroxidation, compared with the nicotine group (p < 0.05). Co-Treatment with ginseng also reduced the expression of apoptotic markers and increased the proliferative indexes in granulosa and theca cells in pre-antral and antral follicles and also in stroma cells, in comparison to the nicotine group (P = 0.001). All above-mentioned alterations following treatment with ginseng were remarkable, especially in the dose of 1 g/kg. Conclusion This study showed ginseng protects folliculogenesis via alteration of hypothalamic- pituitary–gonadal (HPG) axis, induction of proliferation in ovarian somatic cells, reduction of lipid peroxidation, and downregulation of apoptotic markers in the mouse ovary, treated with nicotine.

Nonalcoholic fatty liver disease (NAFLD) is associated with low testosterone levels in serum. The aim of this study was to evaluate the effect of apple vinegar on fertility indices in a rat model of NAFLD. To study this effect, 32 adult male rats were divided into four groups: A-normal diet, B-high-fat diet (HFD), C-apple vinegar and D-HFD plus apple vinegar. At the end of the week 22, the Lee index, serum lipid profiles, liver enzymes, glucose and total antioxidant levels (TAC) in serum were determined. In addition, liver and testis tissue homogenate, histopathology, serum testosterone and sperm parameters were measured and HOMA-IR calculated. Significant reduction in Lee index, serum triglyceride, cholesterol, liver enzymes and glucose levels was observed in vinegar treated group compared with HFD group. Vinegar lowered insulin resistance compared with HFD (p < 0.01). Steatosis in hepatocytes reduced from 56% in HFD group to 20% in group D (p < 0.05). Vinegar caused a significant increase in serum testosterone, improvement in sperm parameters and a reduced germ cell apoptosis (p < 0.05). There was an insignificant increase in TAC levels in the serum and homogenate tissue of liver and testis compared with HFD. This study reports apple vinegar has beneficial effects on male rat fertility indices in an in vivo model of NAFLD.

Nicotine as a toxic agent in cigarette smoke impairs the reproductive system. Sambucus ebulus extract (SEE) is shown to have some beneficial effects such as antioxidant properties. The aim of this study was to evaluate the effects of SEE on the hormones of the pituitary-gonadal axis, lipid peroxidation index, antioxidant enzymes, spermatogenesis, and epididymal sperm parameters in male mice treated with nicotine. Adult male mice were divided into five groups; A: normal saline, B: 1 mg/kg nicotine, C: 1 mg/kg nicotine and 10 mg/kg SEE, D: 1 mg/kg nicotine and 50 mg/kg SEE, D: 1 mg/kg nicotine and 100 mg/kg SEE. Treatments lasted for 35 days. The spermicidal activity of SEE was tested in vitro. Sperm count, motility and morphology were assessed for fertility. Serum testosterone, prolactin and luteinizing hormone (LH) were measured, using ELISA. Serum malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) activity were measured, using colorimetric assays. Spermatogenesis was evaluated by Johnsen's score and morphometry in histological slides. SEE at different doses did not have any spermicidal activity. Sperm parameters were reduced in the nicotine-treated group, compared with controls (P<0.01). Nicotine reduced testosterone and LH levels (P<0.01) and increased prolactin (P<0.01). A hike in MDA and a reduction in SOD activity without change on CAT, were observed in the nicotine group. Nicotine caused hypospermatogenesis. SEE improved most of the above-mentioned parameters, especially in the doses of 50 and 100 mg/kg. Beneficial effects of SEE in the doses of 50 and 100 mg/kg on male reproduction impairment, induced by nicotine might be partly attributed to the reduction of oxidative stress and changes in the hormones of the pituitary-gonadal axis.

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