Progress on the roles of zinc in sperm cryopreservation.

One of the effective methods for the long-term preservation of mammalian genetic resources is the cryopreservation of semen. However, a number of parameters, including diluents, the rate of freezing and thawing, cryoprotectants, etc., can easily alter the survival of frozen-thawed sperm. Numerous studies have documented the addition of a variety of zinc compounds, to the diluents used to cryopreserve sperm. The primary objective of this review is to briefly describe that adding zinc to diluents as an antioxidant significantly enhances frozen-thawed sperm quality. Second, a summary of the present understanding of zinc's molecular mechanism on semen cryopreservation is provided. Thirdly, this study addresses that nanoparticles of zinc can offer suggestions for raising cryopreservation effectiveness.

1α,25(OH)2D3 Promotes the Autophagy of Porcine Ovarian Granulosa Cells as a Protective Mechanism against ROS through the BNIP3/PINK1 Pathway.

Vitamin D (VD) is one of the important nutrients required by livestock; however, VD deficiency is reported to be widespread. Earlier studies have suggested a potential role for VD in reproduction. Studies on the correlation between VD and sow reproduction are limited. The aim of the current study was aimed to determine the role of 1,25-dihydroxy vitamin D3 (1α,25(OH)2D3) on porcine ovarian granulosa cells (PGCs) in vitro to provide a theoretical basis for improving the reproductive efficiency of sows. We used chloroquine (autophagy inhibitor) and reactive oxygen species (ROS) scavenger N-acetylcysteine in conjunction with 1α,25(OH)2D3 to explore the effect on PGCs. The results showed that 10 nM of 1α,25(OH)2D3 increased PGC viability and ROS content. In addition, 1α,25(OH)2D3 induces PGC autophagy according to the gene transcription and protein expression levels of LC3, ATG7, BECN1, and SQSTM1 and promotes the generation of autophagosomes. 1α,25(OH)2D3-induced autophagy affects the synthesis of E2 and P4 in PGCs. We investigated the relationship between ROS and autophagy, and the results showed that 1α,25(OH)2D3-induced ROS promoted PGC autophagy. The ROS-BNIP3-PINK1 pathway was involved in PGC autophagy induced by 1α,25(OH)2D3. In conclusion, this study suggests that 1α,25(OH)2D3 promotes PGC autophagy as a protective mechanism against ROS via the BNIP3/PINK1 pathway.

Expression of ERß induces bovine ovarian granulosa cell autophagy via the AKT/mTOR pathway.

The aim of our study was to determine whether silencing or overexpression of estrogen receptor ß (ERß) regulates cell proliferation, steroidogenesis, autophagy and signalling pathways in bovine ovarian granulosa cells in vitro. In this study, bovine ovarian granulosa cells (BGCs) were cultured and transfected with ERß siRNA (si-ERß) or a plasmid overexpressing ERß (oe-ERß), and CCK-8 kit was used to assess cell proliferation. Real-time PCR was used to measure gene transcription. Western blotting was used to measure protein expression, and a specific kit was used to measure the production of steroid hormones. The results showed the expression level of ERß affects BGC proliferation according to the gene transcription levels of FSHR, CYP19A1, HSD3ß1 and STAR and the production of E2 and P4. ERß was identified as an important nuclear receptor that induced BGC autophagy based on the mRNA and protein expression of autophagy-related genes. Furthermore, the role of ERß in BGC autophagy was confirmed through treatment with rapamycin (RAPA) or 3-methyladenine (3-MA) in BGCs by cotransfection with si-ERß or oe-ERß in BGCs. The results related to AKT/mTOR signalling and phosphorylation suggested that ERß induces BGC autophagy through attenuating AKT/mTOR signalling. In summary, this study demonstrates that silencing or overexpression of ERß regulates BGC proliferation and function and induces BGC autophagy by targeting AKT/mTOR signalling. These data reveal a novel regulatory mechanism of autophagy via ERß and provide insights into the role of autophagy in BGCs.

Function of low back muscle exercise : Preventive effect of refracture analysis of postoperative vertebral fractures.

BACKGROUND: Low back muscles exercise reportedly influence the risk of osteoporotic vertebral fractures. The exact relationship between the low back muscles exercise and the incidence of vertebral refractures remain unclear. OBJECTIVE: To investigate the ability of exercise to strengthen the low back muscles to prevent vertebral refracture after surgery, through clinical analysis of the vertebral fracture risk reduction program. METHODS: In total 152 patients with vertebral fractures who had undergone percutaneous vertebroplasty (PVP) and anti-osteoporosis treatment were randomly divided into observation and control groups. The observation group performed exercises to strengthen the back muscles after surgery. The clinical efficacy and incidence of re-fractures were compared between groups. RESULTS: The observation group had reduced physical dysfunction and pain following surgery. After 3 months, the vertebral body height had significantly decreased (P < 0.05) in the control group but not in the observation group (P > 0.05). In the observation and control groups, the incidence of vertebral refractures was 9.2% (7/76) and 17.1% (13/76), respectively (P < 0.05). CONCLUSION: Postoperative exercise to strengthen the back muscles can improve physical function, relieve pain and promote the recovery of vertebral height; it can also assist in maintaining bone density, thereby significantly reducing the risk of refracture. This approach is safe and effective and can help improve the quality of life in patients with vertebral fractures.