Both PGF and PGE2 produced by the CL increase the survivability of bovine luteal cells by suppressing FAS expression and CASP-mediated apoptosis [11]. In addition, since PGF stimulates P4 production in cultured bovine luteal cells selleck compound [10], luteal PGF is thought to be a luteoprotective factor [11]. On the other hand, both intramuscular PGF injection [37] and endogenous uterine PGF [38] induce luteolysis. Moreover, luteal PGF stimulated by exogenous or uterine PGF has been demonstrated to promote luteolysis in the cow [39]. Therefore, there is still some controversy about whether PGF has different roles in the luteal and uterine origins. In the present study, the viability of luteal cells treated with LH was much higher than that of untreated cells, while the increase in viability caused by LH was decreased by indomethacin (INDO, a COX inhibitor).

In addition, INDO decreased LH-increased PGF production, but did not affect P4 production in bovine luteal cells. The above findings suggest that the luteoprotective actions of LH are also mediated by PG production. Interestingly, although LH in combination with OP stimulated PGF production and LH in combination with INDO stimulated P4 production, both of these combinations decreased luteal cell viability in the present study. These results suggest that luteoprotective roles of LH require both P4 and PGF actions. Further studies are needed to clarify the exact mechanisms of luteoprotective actions of LH. In the present study, LH stimulated the expressions of COX-2 and PGFS but not the expressions of COX-1 and PGES.

In fact, LH stimulated PGF Drug_discovery production but not PGE2 production. Furthermore, LH stimulated the CBR1 enzyme that converts PGE2 to PGF. This could be the reason why the PGE2 concentration in the medium was not increased, although COX-2 expression was stimulated by LH. In addition, since PGF stimulates P4 secretion in bovine luteal cells [10, 11], LH may stimulate P4 secretion not only directly but also by stimulating PGF. However, INDO did not affect LH-increased P4 production in the present study. Since LH has been demonstrated to increase P4 production by a variety of signaling molecules other than PGF [6,7,8], the increased level of P4 production could be mainly induced by LH rather than by LH-stimulated PGF. In summary, LH stimulated P4 and PGF production but not PGE2 production. LH increased luteal cell viability, and this luteoprotective action of LH was inhibited by OP as well as by INDO. The overall findings suggest that LH protects CL function by stimulating the production of P4 and PGF in cows.