中文摘要：

目的探讨全反式维A酸（at—RA）抑制光老化皮肤基质金属蛋白酶（MMP）-3和MMP-13表达的受体机制。方法中长波紫外线照射ICR小鼠12周，建立皮肤光老化动物模型，按照实验分组进行at—RA、维A酸受体（RAR）／维A酸X受体（RXR）的激动剂／拮抗剂干预后，HE染色观察皮肤组织病理学的改变；Western blot检测MMP-3和MMP-13的蛋白表达水平；碱水解法检测皮肤胶原蛋白的含量。结果与模型对照组相比，at—RA组、RAR激动剂组胶原蛋白含量增多，MMP-3和MMP-13表达量明显减少（P均〈0．01），而RXR激动剂组与模型对照组的差异无统计学意义；at—RA／RAR激动剂＋RAR拮抗剂组较at—RA／RAR激动剂组胶原蛋白含量减少，MMP-3和MMP-13表达量显著增多（P均〈0．01），而at—RA＋RXR拮抗剂组与at—RA组的差异无统计学意义。结论at—RA可通过RAR下调MMP-3和MMP-13蛋白的表达，抑制光老化皮肤胶原的降解。

英文摘要：

Objective To investigate the receptor mechanisms of all-trans retinoic acid （at-RA）-induced inhibition of matrix metalloproteinase （MMP）-3 and MMP-13 in photoaged skin. Methods The photoaged model was established by irradiation of ICR mice with UVA and UVB for 12 weeks. The photoaged mice were treated topically with at-RA, retinoic acid receptor （RAR） or retinoid X receptor （RXR） agonist/antagonist. HE staining was used to evaluate the histopathologic changes in the skin while expression levels of MMP-3 and MMP-13 protein were analyzed by Western blot. The collagen contents were measured by the method of alka- line hydrolysis. Results Compared with vehicle controls, the collagen contents were increased in mice treated with either at-RA or RAR agonist, while the expression levels of MMP-3 and MMP-13 were reduced significantly （ all P 〈 0. 01 ）. In contrast, the expression levels of MMP-3 and MMP-13 were no significant differences between RXR agonist and vehicle controls. The collagen content was lower in mice treated with at-RA/RAR agonist plus RAR antagonist group than at-RA/RAR agonist treatment, whereas the expression levels of MMP-3 and MMP-13 were significantly higher in at-RA/RAR agonist plus RAR antagonist group than at-RA/RAR agonist treatment （all P 〈 0. 01 ）. However, the expression levels of MMP-3 and MMP- 13 were no significant differences between at-RA plus RXR antagonist group and at-RA group. Conclusion At-RA inhibits the degradation of collagen via RAR to downregulate the expressions of MMP-3 and MMP-13 in photoaged skin.