Roger, got it. The problem is that I went to government schools, so can you translate it for me please?
Sure.
“Prostaglandin, a potent bone-resorbing agent, is synthesized in osteoblast-like cells. Since vitamin K reportedly plays an important role in (viscosity, clotting &) bone metabolism, we investigated the effects of vitamin K2 (menatetrenone) on PGE2 production by human osteoblast-like periosteal cells. “
The above is the background and introduction. Prostaglandin is made in bone cells and is a bone resorbing agent. Bone resorbtion releases calcium in to the blood.
This vitamin, chemical name menatetrenone, is known to affect bone metabolism, so they did experiments to see if it affects production if prostaglandins in bone cells. It specifies the cells used for the experiments, periosteal cells. (The experiments are done with cells in culture).
“In cells incubated with menatetrenone (1 microgram/mL = 2.25 x 10(-6) M) for 2 days, PGE2 production was reduced to 50% of that in untreated control cells.”
When cells were grown with the vitamin, prostaglandin E2 synthesis was decreased by half. The concentration of vitamin and length of exposure time are given.
The next experiments look at the mechanism whereby prostaglandin synthesis was inhibited.
“In one of these menatetrenone at doses of 0.5-10 micrograms/mL dose dependently inhibited the calcium ionophore A23187-induced release of arachidonic acid (AA) from membrane phospholipids, and in the other the conversion of AA to PG was inhibited, as evidenced by the PG-synthesizing activity in the homogenates of menatetrenone-treated cells with AA being lower than that in untreated cells. The inhibitory effect was almost identical to that for PG production.”
The vitamin caused two steps in the process of synthesizing prostaglandin to be affected, the release of arachidonic acid and enzymatic reaction that turns it in to prostaglandin. These inhibitory responses were dose-dependent, meaning the more vitamin added to the cell culture, the greater the inhibition.
“This study shows that menatetrenone inhibited PGE2 release from cells by inhibiting both PG production steps, AA release from the membrane and PG synthesizing activity with AA. Inhibition of PGE2 production by menatetrenone might be important in improving bone metabolism.”
This concluding section reiterates the findings and suggests a possible use for the vitamin.