@stag
While it was suspected by the authors that progesterone may bind to endotoxin directly, another mechanism of its protection may be by increasing the ability of albumin to bind LPS:
One of estrogen's effects is to lower the amount of albumin in the blood. Estrogen causes the liver to synthesize less albumin, partly by causing the messenger RNA to be destabilized and degraded. (Iron can have some similar effects on liver RNA.) When there isn't enough albumin in the blood, water moves from the blood into the tissues. Albumin binds oily substances, and its conformation seems to be opened when it binds them. Progesterone is known to adsorb strongly to proteins--it has been called a "cardinal adsorbant," meaning that it can bind in ways that cause the protein's adsorptive capacity to change I believe that progesterone and pregnenolone oppose estrogen in many ways, but the amazing speed with which they can cause major structural changes in the soft tissues convinces me that one of their first sites of action is the albumin molecule, causing its conformation to open in such a way that it is able to more strongly bind water molecules. This physical change in albumin would change the blood's osmotic/oncotic pressure, causing water to flow into capillaries. As the edema is reduced, oxygenation is more efficient, because the pathway for oxygen diffusion becomes shorter.
Albumin has been described as a first line of defense against toxins, since it binds them until the liver is able to degrade them chemically. Progesterone, pregnenolone, and cholesterol are known to increase thc organism's resistance to a great variety of toxins. (Selye coined the name "catatoxic steroids" to describe steroids of this type.) If these steroids bind to albumin in a way that opens the protein to increase its binding capacity, that single process could explain the "catatoxic" effect, as well as the anti-edema effect.
Ray Peat, From PMS to Menopause: Female Hormones in Context
