Fowler Ashley J, Sheu Mary Y, Schmuth Matthias, Kao Jack, Fluhr Joachim W, Rhein Linda, Collins Jon L, Willson Timothy M, Mangelsdorf David J, Elias Peter M, Feingold Kenneth R
Department of Dermatology, University of California, San Francisco, USA.
J Invest Dermatol. 2003 Feb;120(2):246-55. doi: 10.1046/j.1523-1747.2003.12033.x.
Activators of liver X receptors (LXR) stimulate epidermal differentiation and development, but inhibit keratinocyte proliferation. In this study, the anti-inflammatory effects of two oxysterols, 22(R)-hydroxy-cholesterol (22ROH) and 25-hydroxycholesterol (25OH), and a nonsterol activator of LXR, GW3965, were examined utilizing models of irritant and allergic contact dermatitis. Irritant dermatitis was induced by applying phorbol 12-myristate-13-acetate (TPA) to the surface of the ears of CD1 mice, followed by treatment with 22ROH, 25OH, GW3965, or vehicle alone. Whereas TPA treatment alone induced an approximately 2-fold increase in ear weight and thickness, 22ROH, 25OH, or GW3965 markedly suppressed the increase (greater than 50% decrease), and to an extent comparable to that observed with 0.05% clobetasol treatment. Histology also revealed a marked decrease in TPA-induced cutaneous inflammation in oxysterol-treated animals. As topical treatment with cholesterol did not reduce the TPA-induced inflammation, and the nonsterol LXR activator (GW3965) inhibited inflammation, the anti-inflammatory effects of oxysterols cannot be ascribed to a nonspecific sterol effect. In addition, 22ROH did not reduce inflammation in LXRbeta-/- or LXRalphabeta-/- animals, indicating that LXRbeta is required for this anti-inflammatory effect. 22ROH also caused a partial reduction in ear thickness in LXRalpha-/- animals, however (approximately 50% of that observed in wild-type mice), suggesting that this receptor also mediates the anti-inflammatory effects of oxysterols. Both ear thickness and weight increased (approximately 1.5-fold) in the oxazolone-induced allergic dermatitis model, and 22ROH and GW3965 reduced inflammation by approximately 50% and approximately 30%, respectively. Finally, immunohistochemistry demonstrated an inhibition in the production of the pro-inflammatory cytokines interleukin-1alpha and tumor necrosis factor alpha in the oxysterol-treated sites from both TPA- and oxazolone-treated animals. These studies demonstrate that activators of LXR display potent anti-inflammatory activity in both irritant and allergic contact models of dermatitis, requiring the participation of both LXRalpha and LXRbeta. LXR activators could provide a new class of therapeutic agents for the treatment of cutaneous inflammatory disorders.
肝X受体(LXR)激活剂可刺激表皮分化与发育,但抑制角质形成细胞增殖。在本研究中,利用刺激性和过敏性接触性皮炎模型,检测了两种氧化甾醇,即22(R)-羟基胆固醇(22ROH)和25-羟基胆固醇(25OH),以及一种LXR的非甾醇激活剂GW3965的抗炎作用。通过将佛波醇12-肉豆蔻酸酯-13-乙酸酯(TPA)涂抹于CD1小鼠耳部表面诱导刺激性皮炎,随后分别用22ROH、25OH、GW3965或单独的赋形剂进行处理。单独使用TPA处理可使耳部重量和厚度增加约2倍,而22ROH、25OH或GW3965可显著抑制这种增加(减少超过50%),其抑制程度与0.05%氯倍他索处理相当。组织学检查还显示,氧化甾醇处理的动物中TPA诱导的皮肤炎症明显减轻。由于用胆固醇进行局部处理并未减轻TPA诱导的炎症,且非甾醇LXR激活剂(GW3965)可抑制炎症,因此氧化甾醇的抗炎作用不能归因于非特异性甾醇效应。此外,22ROH在LXRβ-/-或LXRαβ-/-动物中并未减轻炎症,表明LXRβ是这种抗炎作用所必需的。然而,22ROH在LXRα-/-动物中也使耳部厚度部分降低(约为野生型小鼠中观察到的50%),提示该受体也介导氧化甾醇的抗炎作用。在恶唑酮诱导的过敏性皮炎模型中,耳部厚度和重量均增加(约1.5倍),22ROH和GW3965分别使炎症减轻约50%和约30%。最后,免疫组织化学显示,在TPA和恶唑酮处理动物的氧化甾醇处理部位,促炎细胞因子白细胞介素-1α和肿瘤坏死因子α的产生受到抑制。这些研究表明,LXR激活剂在刺激性和过敏性接触性皮炎模型中均显示出强大的抗炎活性,且需要LXRα和LXRβ的共同参与。LXR激活剂可为治疗皮肤炎症性疾病提供一类新型治疗药物。