In:
British Journal of Pharmacology, Wiley, Vol. 131, No. 6 ( 2000-11), p. 1172-1178
Kurzfassung:
This study investigated the effect of magnolol, a compound purified from Magnolia officinalis , on glucocorticoid production by primary adrenal cell culture. Magnolol increased corticosterone secretion in a dose‐dependent manner, this effect being maximal at 40 μ M . A similar effect was seen in a minced adrenal gland system. 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. 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. The stimulatory effect of magnolol on steroidogenesis apparently requires new protein synthesis, since cycloheximide inhibited magnolol‐induced corticosterone production by 50%. Although other studies have shown that high concentrations of magnolol inhibit acyl‐CoA: cholesterol acyltransferase and 11β‐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 . British Journal of Pharmacology (2000) 131 , 1172–1178; doi: 10.1038/sj.bjp.0703669
Materialart:
Online-Ressource
ISSN:
0007-1188
,
1476-5381
DOI:
10.1038/sj.bjp.0703669
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2000
ZDB Id:
2029728-2
SSG:
15,3
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