LIF regulates the expression of miR-27a-3p and HOXA10 in bovine endometrial epithelial cells via STAT3 pathway.

LIF is crucial in regulating embryo implantation, while HOXA10 is a marker gene for uterine receptivity. However, the specific mechanism of LIF regulating HOXA10 during cow embryo implantation has not been fully understood. To address this knowledge gap, the experiment involved treating bovine endometrial epithelial cells (BEECs) with LIF to investigate the relationship between LIF, miRNA, and HOXA10.

Progesterone regulates inflammation and receptivity of cells via the NF-κB and LIF/STAT3 pathways.

A high concentration of blood ammonia can lead to failure of early embryo implantation in dairy cows. Progesterone (P4) is an important hormone that regulates the changes of uterine receptivity and participates in pregnancy during early implantation. However, whether P4 alleviates the harmful effects of blood ammonia is unknown.

LRH-A3 and HCG increase pregnancy rate during timed artificial insemination in dairy cows.

The objective of this study was to use luteinizing hormone-releasing hormone A3 (LRH-A3) and human chorionic gonadotrophin (HCG) to improve pregnancy rate of dairy cows during timed artificial insemination (TAI). In experiment 1, the TAI process (0 d, GnRH, 100 μg; 7 d, PGF2α, 0.4 mg; 56 hr, GnRH, 100 μg; 16 hr, AI) was applied to 160 dairy cows on 50th and 60th days after parturition respectively.

Pharmacological inhibition of TLR4/NF-κB with TLR4-IN-C34 attenuated microcystin-leucine arginine toxicity in bovine Sertoli cells.

This study investigated the pharmacological inhibition of the toll-like receptor 4 (TLR4) genes as a measure to attenuate microcystin-LR (MC-LR) reproductive toxicity. Bovine Sertoli cells were pretreated with TLR4-IN-C34 (C34) for 1 hour. Thereafter the pretreated and non-pretreated Sertoli cells were cultured in medium containing 10% heat-activated fetal bovine serum + 80 μg/L MC-LR for 24 hours to assess the ability of TLR4-IN-C34 to attenuate the toxic effects of MC-LR.