1. This study investigated the effect of
magnolol, a compound purified from Magnolia officinalis, on
glucocorticoid production by primary adrenal cell culture. 2.
Magnolol increased
corticosterone secretion in a dose-dependent manner, this effect being maximal at 40 microM. A similar effect was seen in a minced adrenal gland system. 3. In
magnolol-treated cells, the number and total area of cytoplasmic lipid droplets were reduced, suggesting a high utilization rate of
cholesterol esters stored in lipid droplets. In control cells, the
capsule of the lipid droplet was clearly delineated by immunostaining with antibody A2, whereas capsular staining was discontinuous or undetectable following
magnolol treatment. The percentage of decapsulated cells increased significantly from 20% in the control group to 80% in the
magnolol-treated group. 4.
Magnolol-induced steroidogenesis was not mediated either via the traditional
ACTH-
cyclic AMP-
protein kinase A pathway or by
protein kinase C, since the intracellular
cyclic AMP level did not change and inhibition of
protein kinase A or C did not block the action of
magnolol. Furthermore,
calcium/calmodulin-dependent protein kinase II was not involved in
magnolol-induced steroidogenesis. 5. The stimulatory effect of
magnolol on steroidogenesis apparently requires new
protein synthesis, since
cycloheximide inhibited
magnolol-induced
corticosterone production by 50%. 6. Although other studies have shown that high concentrations of
magnolol inhibit
acyl-CoA: cholesterol acyltransferase and
11 beta-hydroxysteroid dehydrogenase in a cell-free system, our data show that, in adrenal cell cultures, low concentrations of
magnolol have a stimulatory effect on steroidogenesis, and the
glucocorticoid produced may explain the effective control of
asthma by Magnolia officinalis.