Thyroid hormones have an in uence on the connectivedermal blood ow as a consequence of increased metatissue biology of the skin and, theoretically, topically bolic rate and decreased systemic vascular resistance applied thyroid hormones or hormone analogues could have and are thus not attributable to a direct action of TH a stimulatory eVect on collagen synthesis. In this investion cells in the skin (2-5). However, it is also known gation the eVect of topical tri-iodothyroaceti c acid (Triac) that the connective tissue biology of the skin is sensitive and other thyroid hormone analogues were tested for their to alterations in thyroid hormone status (3) and the eVect in preventing betamethasone-indu ced skin atrophy in presence of intracellular receptors ( TRs) for thyroid the normal haired mouse. Triac, tri-iodoproprioni c acid hormones in human skin, in both dermal and epidermal ( Triprop) and the synthetically developed thyroid hormone parts, have been demonstrate d (6-10). analogue KB-026 and 2 diVerent Triac cream formulationsInformation concerning the mechanism of action of TH were applied along with betamethasone on shaved mouse in broblasts, especially in regulation of collagen producskin. Triac in daily doses of 1 nmol/cm2 and higher was tion, is limited. In one study by Rycker et al., thyroid able to block the betamethasone-induce d skin atrophy in hormone administration diminished collagen production mice skin. In high doses, Triprop and KB-026 also had a in cultured broblasts (9). Although a vast number of blocking eVect. Triac alone had a stimulatory eVect on studies on thyroid hormone action in organs such as liver, dermal thickness. This study indicates that thyroid hormone heart, pituitary, brain and adipose tissue have been peranalogues may be used to prevent corticosteroid-induce d formed, no studies have been undertaken to investigate skin atrophy. Keywords: animal model; skin thickness; the activity of topical TH in glucocorticoid-treated skin. normal haired mouse.Moreover, as TRs are part of a larger superfamily of nuclear receptors, which comprises the receptors for gluco-
Previously we demonstrated the stimulation of collagen synthesis in triiodothyroacetic acid (TRIAC)-topically treated human and mice. In the present study, we have evaluated the dose response effect of thyroid hormone (TH) analogues and tretinoin on glucocorticoid-induced skin atrophy in a haired mouse model. For this investigation, we treated haired mice twice daily for 7 days with various topically administered doses of TRIAC, triiodothyronine-sodium salt (T(3)-Na), diiodothyroacetic acid (DIAC), 3,5-diiodothyropropionic acid (DITPA), and tretinoin with 0.2 mM betamethasone17-valerate (BM), or with the vehicle as a control group. We also investigated a combination of commercial betamethasone dipropionate (BD) 0.05% cream and various doses of TRIAC on mouse skin. TRIAC was able to reverse the skin atrophy by 25% in a daily dose of 1 nmol/cm(2) in the presence of 0.2 mM BM (p < 0.05). Neither other TH analogues nor TRIAC in lower and higher concentrations had a significant inhibitory effect on dermal atrophy (p > 0.05). A combination of 0.2 mM BM and 10 nmol/cm(2) TRIAC was able to prevent dermal atrophy by 18%. The addition of TRIAC to 0.05% BD cream in a final concentration of 0.1% was able partially to reverse the dermal atrophy by 15% (p < 0.05). TRIAC alone in a concentration of 1,000 nmol/cm(2) stimulated dermal proliferation by 34% (p < 0.05). Other TH analogues alone had no stimulatory effect on dermal proliferation. Tretinoin 0.8 mM was able to inhibit dermal atrophy by 20% (p < 0.05) and had an effect on dermal thickness of 85% (p < 0.05). However, severe side effects with edema, erythema, and scaling were commonly observed in all tretinoin-treated mouse skin, which could partly explain the increase in dermal thickness. In contrast, no skin side effects were observed after treatment with TRIAC. This study indicates that TRIAC may have a therapeutic effect on BM-induced dermal atrophy in mouse skin and a direct stimulatory effect on dermal proliferation when given alone.
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