Effect of aqueous Nigella sativa extract on the functional parameters of post-thaw human spermatozoa during vitrification.

OBJECTIVE: Sperm vitrification leads to the production of reactive oxygen species (ROS) that can damage the functional parameters of sperm. The present study aimed to investigate the antioxidant effect of Nigella sativa extract on motility, plasma membrane function, mitochondrial membrane potential (MMP), DNA damage, and intracellular ROS production. METHODS: A total of 20 sperm samples were used. Samples were divided into six experimental groups, including groups with aqueous extract from N. sativa seeds at concentrations of 1% to 6%, a cryopreserved control group, and a fresh control group. RESULTS: Statistical analysis showed significantly higher total sperm motility at concentrations of 3% to 6% than in the vitrified semen control group. Additionally, progressive motility and all motion characteristics at all concentrations were significantly higher than in the vitrified semen control group. The presence of N. sativa seed extract also improved the quality of the sperm parameters assayed in all experimental groups (1%-6%; intracellular ROS production, DNA damage, MMP, and sperm membrane function) compared to the control group. CONCLUSION: Higher concentrations of N. sativa led to improvements in all sperm parameters and sperm quality. These findings indicate that N. sativa seed extract is effective for improving the quality of sperm after vitrification.

Comparative effects of estrogen and silibinin on cardiovascular risk biomarkers in ovariectomized rats.

BACKGROUND: Silibinin is a polyphenolic compound that could modulate estrogen receptor activation. Vascular dysfunction is considered a key initiator in atherosclerosis and may occur in the postmenopausal period. This manuscript compares estrogen and silibinin's impacts on factors that change endothelial function in ovariectomized (OVX) rats. METHODS: 32 female Wistar rats were subdivided into control; OVX; OVX + estrogen (1 mg/kg/day); and OVX + silibinin (50 mg/kg/day) groups. After the experimental period, lipid profile, atherogenic indices, and histopathology of endothelium were monitored. The vascular oxidative stress, adhesion molecules, inflammatory cytokine levels, nitric oxide (NO), angiotensin-II (Ang-II), and endothelin-1 (ET-1) were also analyzed. RESULTS: Silibinin treatment, similar to estrogen, significantly normalized the adverse changes of OVX on vascular function, including improved lipid profile and oxidative stress, increased endothelial nitric oxide synthase (eNOS) expression, diminished inflammatory status, and reduced adhesion molecule levels, ET-1 and Ang-II substances. Our findings also revealed that the administration with estrogen or silibinin resulted in a normal endothelium layer in the aorta tissues of OVX rats. CONCLUSION: Estrogen and silibinin have similar effects in improving vascular function. These treatments' protective impacts on vasculature indicate their potential benefits on the cardiovascular system in the postmenopausal period.

Silibinin exerts anti-cancer activity on human ovarian cancer cells by increasing apoptosis and inhibiting epithelial-mesenchymal transition (EMT).

BACKGROUND: Silibinin, the principal flavonoid derived from milk thistle seeds, has been demonstrated to have strong inhibitory effects against human malignancies. The inhibitory function of silibinin on ovarian cancer, however, is not fully identified. In this essay, both in vivo and in vitro investigations were conducted to survey the silibinin's blocking effects on ovarian cancer. METHODS: The impacts of silibinin on two ovarian cancer cell lines, SKOV-3 and A2870, were determined by evaluating cell viability, migration, invasion, and apoptosis. Q-RT-PCR and western blotting techniques were carried out to explore the protein levels of signaling pathway markers. A mouse xenograft model was utilized to determine the silibinin efficacy in inhibiting tumor growth. RESULTS: After cell treatment with silibinin, cell viability, migration, and invasion were appreciably inhibited in cancer cell lines, but cell apoptosis was promoted. Also, silibinin reversed the epithelial-mesenchymal transition (EMT) mechanism by inducing E-cadherin expression and reducing N-cadherin and vimentin expression, suppressing the levels of regulators related to EMT such as Snail, Slug, and ZEB1 transcription factors, and also decreasing PI3K/AKT, Smad2/3, and ß-catenin intermediate molecules in vitro. Silibinin effectively ameliorated tumor growth in vivo. CONCLUSION: silibinin could be considered a potent agent against ovarian cancer based on the results.