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Abstract
Clobetasol-17-propionate (CP), a synthetic glucocorticoid (GC), reduced skin thickness
in rats. Both the subcutaneous injection and topical applications of RU 486 counteracted
CP-induced reduction in skin thickness. Topical application of the CP cream completely
inhibited the ear edema produced by croton oil. A less potent GC, hydrocortisone-17-butyrate,
also inhibited ear edema. This antiinflammatory effect was not abolished by the subcutaneous
injection or topical application of RU 486. These observations suggest that GC-induced
skin atrophy is mediated by glucocorticoid receptors (GRs), while the inhibition of
croton oil-induced inflammation by GC is primarily related to the direct effects of
GC, which are not mediated by GRs. Our findings suggest that RU 486 inhibits the atrophogenic
effect of GCs without interfering with their antiinflammatory effect. Dissociation
of antiinflammatory and atrophogenic activity of GC seems favorable in treating inflammatory
skin diseases lacking epidermal proliferation.
Keywords
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Article info
Publication history
Accepted:
February 10,
1995
Received in revised form:
February 10,
1995
Received:
August 23,
1994
Identification
Copyright
© 1995 Published by Elsevier Inc.
