Aqueous Extract of Adansonia digitata reversed Cotton Seed Extract-Induced Testicular Damage in Wistar rats.

OBJECTIVE: Infertility is the inability of sexually active couples without using birth control to get pregnant after one year of uninterrupted sexual intercourse. Cotton Seed Extract (CSE) has been linked to male infertility by causing oxidative damage to the testes due to the action of its active component, Gossypol. Adansonia digitata has been known to have many medically useful properties, including antioxidant effects. This study aimed at evaluating the effects of Adansonia digitata on Cottonseed extract-induced testicular damage. METHODS: Forty (40) Adult male Wistar rats were divided into 8 groups of five rats per group (n=5). Group 1 served as the control and received 0.5 ml of phosphate buffer orally; Group 2 received 800 mg/kg b.wt A. digitata orally; Group 3 received 300 mg/kg b.wt Vitamin E only orally; Group 4 received 60 mg/kg b.wt CSE intraperitoneally; Group 5 received 20 mg/kg b.wt CSE intraperitoneally; Group 6 received 60 mg/kg b.wt CSE intraperitoneally and 800 mg/kg b.wt A. digitata orally; Group 7 received 20 mg/kg b.wt CSE intraperitoneally and 800 mg/kg b.wt A. digitata orally; Group 8 received 60 mg/kg b.wt CSE intraperitoneally and 300 mg/kg Vit. E orally. It was administered for 21 days. The testes and epididymis were dissected following abdominal incision. The epididymis was used for semen analysis while the testes was processed for histological analysis and biochemical assay. All the data was analyzed by ANOVA, using the SPSS version 17.0 software. A p<0.05 was considered significant. RESULTS: CSE administration caused significant (p<0.05) decrease in sperm count, found in the group treated with CSE only. However, the Administration of A. digitata caused significant increase (p<0.05) in sperm count, G6PDH, LDH, GPx and SOD; however, MDA levels were decreased. Histological observations showed a decrease in the number of Spermatogonia and differentiating cells in the testes of rats treated with CSE. CONCLUSIONS: The results obtained revealed the antioxidant ability of A. digitata in counter-acting the testicular damage caused by CSE administration.

Quercetin modulates granulosa cell mRNA androgen receptor gene expression in dehydroepiandrosterone-induced polycystic ovary in Wistar rats via metabolic and hormonal pathways.

Background It is estimated that about 5-10% of women suffer from polycystic ovarian syndrome (PCOS) which is a major cause of female reproductive dysfunction. This study examined the role of quercetin on dehydroepiandrosterone (DHEA)-induced PCO in Wistar rats. Methods Twenty-eight pre-pubertal female Wistar rats that are 21 days old weighing 16-21 g were sorted into four groups (n = 7). Group I served as control and was given distilled water only, Group II were injected with 6 mg/100 g BW of DHEA in 0.2 mL of corn oil subcutaneously, Group III received 100 mg/kg BW of quercetin orally and Group IV received 6 mg/100 g BW of DHEA in 0.2 mL of corn oil subcutaneously and 100 mg/kg BW of quercetin orally. Rats were sacrificed after 15 days by cervical dislocation method. Blood samples and ovaries were collected for hormonal, biochemical, and histopathological analysis and expressions of mRNA androgen receptor gene were determined using RT-qPCR. All data were analysed using one-way ANOVA. Results A significant decrease (p < 0.05) in the antioxidant and metabolic enzyme activity in the DHEA treated group was observed when compared with control. DHEA co-administration with quercetin showed a significant decrease in malondialdehyde and cytokines when compared with DHEA treated group. Also a significant increase in progesterone, metabolic and antioxidant enzyme activity was observed. The histopathology demonstrates a reduction in cystic and atretic cells, improved expression of BCl2, E-Cadherin and a decrease in Bax. Conclusions Quercetin alleviated DHEA-induced PCO. These effects could be attributed to its antioxidant property.

Vitamin C suppresses ovarian pathophysiology in experimental polycystic ovarian syndrome.

BACKGROUND: Polycystic ovary syndrome (PCOS), also known as the Stein-Leventhal syndrome is one of the most common causes of anovulation, infertility and hyperandrogenism in women, affecting between 5-10 % of women of reproductive age (12-35 years) worldwide. Despite substantial effort to define the cause of PCOS, its pathophysiology remains poorly understood. Consequently, determining the mechanisms of PCOS and the possible treatment is the major goal of medical research in endocrine and reproductive physiology. AIM: To investigate the mechanism of ovarian metabolic changes in dehydroepiandrosterone (DHEA)-induced polycystic ovary in Wistar rats treated with vitamin C. METHODS: Twenty-eight immature female Wistar rats weighing (16-21 g) were randomly divided into four groups (n = 7/group): group I served as control and was given water, group II were injected with DHEA (6 mg/100 g in 0.2 ml corn oil subcutaneously to induce PCOS condition), group III received 150 mg/kg BW of Vitamin C orally, group IV were co-administered with 6 mg/kg BW DHEA in 0.2 ml of corn oil subcutaneously and 150 mg/kg BW of Vitamin C orally. All treatments lasted for 15 days. Twenty-four hours after the last administration, the rats were sacrificed by cervical dislocation. Blood samples and ovaries were collected for reproductive hormonal analysis, biochemical and histopathological analysis. The expressions of mRNA androgen receptor gene in the ovary were determined by real-time reverse transcriptase polymerase chain reaction. All data were analysed using one-way ANOVA. RESULTS: There was a significant decrease (p < 0.05) in the antioxidant and metabolic enzyme activity in the DHEA treated group compared with the control group. DHEA co-administration with Vitamin C showed a significant decrease in Malondialdehyde, cytokines and Estrogen and a significant increase (p < 0.05) in antioxidant and metabolic enzymes compared with DHEA treated group only. The histopathological evaluation demonstrates a reduction in cystic and atretic ovaries, increased expression of Bcl2 and E-Cadherin with a reduction in Bax expression in the group co-administered with DHEA and Vitamin C. The DHEA group showed overexpression of mRNA Androgen Receptor gene in the ovaries compared to the control group. CONCLUSION: This study shows that Vitamin C plays a protective role against DHEA-Induced Polycystic Ovary in Wistar rats via its antioxidant and anti-apoptotic mechanisms.