• 대한화장품학회지
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• 제23권3호
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• pp.9-23
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• 1997

Retinoids are essential regulators of spithelial cell growth and celluar differentiation. They are also known to be effective in photoaging. It was reported that topical application of retinoic acid improves facial wrinkle carsed by collagen synthesis reduction in photodamaged skin. Collagen synthesis by retinoic acid may contribute to the wrinkle effacement. Since celluar retinoic acid binding protein II is slsctively induced in human skin and dermal fibroblasts in vitro by retinoic acid, this response can be used to mesure retinoids potency and activity. In order to know the activity of retinoids and their relations with collagen synthesis, we treated dermal fibroblasts with retinoids for 48 hours at 10-6-10-7M and measured CRABPII mRNA level by quantitative Nortern blotting. We also measured the rate of collagen systhesis by retinoids using 3-dimensional dermal equivalent. CRABPII mRNA level was increased 3-fold by retinoic acid, 2.1-fold by retinol and 1.4-fold by retinaldehyde. Collagen systhesis was increased 34% by all-trans retinioc acid, 26% by retinol, 17% by retinaldehyde and 7% by retinyl palmitate. From the above results, retinoids were found to be a potent indecers of CRABPII mRNA and collagen synthesis. Though retinoic acid was the most effective, its use has been restricted because of the side effects. Instead, retinol can be a best candidate in cosmetics for the treatment of photodamaged skin in terms of efficacy and safety.

• 대한화장품학회지
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• 제48권1호
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• pp.77-85
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• 2022

레틴알(RA)은 레티놀과 레티노익애씨드의 중간체로 비타민A 유도체이며 주름개선 효과가 우수하다. 본 연구에서는 drug-in-cyclodextrin-in-liposome (DCL)을 이용하여 레틴알의 안정성을 높였다. 레틴알과 hydroxypropyl-β-cyclodextrin (HP-β-CD) 복합체를 동결건조 방식으로 제조하였고, UV-Vis 분광법, FT-IR 및 SEM 이미지로 레틴알의 포접 여부를 확인하였다. 레틴알과 HP-β-CD의 비율이 1 : 15 (w/w)일 때 약 95.6% 포집되었다. 레틴알-HP-β-CD 복합체는 호모믹서 및 마이크로플루다이저로 리포좀에 담지시켰으며, 평균 입자 크기는 215.3 ± 4.2 nm, 제타포텐셜 -33.2 ± 1.5 mv로 나타났다. 레틴알의 분해 안정도 평가에서, 물에서 레틴알-HP-β-CD-리포좀의 레틴알 감소율은 1.8%로 레틴알-리포좀(5.8%), 레틴알-HP-β-CD복합체(9.7%), 레틴알 단독(37.6%)보다 높게 나타났다. 레틴알-HP-β-CD-리포좀이 함유된 크림(0.05% RA 함유)을 제조하여, 미간, 이마, 목, 눈가, 입가, 팔자 주름개선 효능 및 피부 치밀도를 2 ~ 4 주간 평가하였다. 그 결과 레틴알크림은 피부 자극 없이 유의한 주름 개선 효과를 보였다. 결론적으로, DCL시스템을 이용한 이중 안정화 기술은 레틴알의 안정화를 높여 피부 주름 개선 효과에 기여함을 확인하였다.

• Molecules and Cells
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• 제44권8호
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• pp.613-622
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• 2021

In vertebrate eyes, the retinal pigment epithelium (RPE) provides structural and functional homeostasis to the retina. The RPE takes up retinol (ROL) to be dehydrogenated and isomerized to 11-cis-retinaldehyde (11-cis-RAL), which is a functional photopigment in mammalian photoreceptors. As excessive ROL is toxic, the RPE must also establish mechanisms to protect against ROL toxicity. Here, we found that the levels of retinol dehydrogenases (RDHs) are commonly decreased in phosphatase tensin homolog (Pten)-deficient mouse RPE, which degenerates due to elevated ROL and that can be rescued by feeding a ROL-free diet. We also identified that RDH gene expression is regulated by forkhead box O (FOXO) transcription factors, which are inactivated by hyperactive Akt in the Pten-deficient mouse RPE. Together, our findings suggest that a homeostatic pathway comprising PTEN, FOXO, and RDH can protect the RPE from ROL toxicity.

• Molecules and Cells
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• 제38권11호
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• pp.998-1006
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• 2015

Retinols are metabolized into retinoic acids by alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (Raldh). However, their roles have yet to be clarified in hepatitis despite enriched retinols in hepatic stellate cells (HSCs). Therefore, we investigated the effects of retinols on Concanavalin A (Con A)-mediated hepatitis. Con A was injected into wild type (WT), Raldh1 knockout ($Raldh1^{-/-}$), $CCL2^{-/-}$ and $CCR2^{-/-}$ mice. For migration study of regulatory T cells (Tregs), we used in vivo and ex vivo adoptive transfer systems. Blockade of retinol metabolism in mice given 4-methylpyrazole, an inhibitor of ADH, and ablated Raldh1 gene manifested increased migration of Tregs, eventually protected against Con A-mediated hepatitis by decreasing interferon-${\gamma}$ in T cells. Moreover, interferon-${\gamma}$ treatment increased the expression of ADH3 and Raldh1, but it suppressed that of CCL2 and IL-6 in HSCs. However, the expression of CCL2 and IL-6 was inversely increased upon the pharmacologic or genetic ablation of ADH3 and Raldh1 in HSCs. Indeed, IL-6 treatment increased CCR2 expression of Tregs. In migration assay, ablated CCR2 in Tregs showed reduced migration to HSCs. In adoptive transfer of Tregs in vivo and ex vivo, Raldh1-deficient mice showed more increased migration of Tregs than WT mice. Furthermore, inhibited retinol metabolism increased survival rate (75%) compared with that of the controls (25%) in Con A-induced hepatitis. These results suggest that blockade of retinol metabolism protects against acute liver injury by increased Treg migration, and it may represent a novel therapeutic strategy to control T cell-mediated acute hepatitis.