糖皮质激素受体与褪黑素受体在斑秃皮损中的表达

目的:检测斑秃(AA)患者皮损及健康头皮标本中糖皮质激素受体(GR)和褪黑素受体(MR)的表达.方法:用免疫组化法检测15例AA患者和16例正常对照组GR-α、GR-β、MR1的表达.结果:GR-α的表达在AA组明显强于健康组(P＜0.05);在毛囊生长期和静止期细胞中AA组GR-α的表达强于健康组(P＜0.01);GR-β在AA组与健康组的表达无统计学意义(P＞0.05);MR1在AA组表皮层表达弱于健康组(P＜0.05);在真皮间质炎细胞中AA组高于健康组,并与间质炎细胞分布关系密切(P＜0.05).结论:GR-α不仅在正常毛发生长中起着重要作用,而且通过对毛囊生长期和静止期的影响参与了斑秃的发生.     

糖皮质激素受体与某些免疫相关性皮肤病

系统或外用糖皮质激素是皮肤科临床最常用的治疗手段,糖皮质激素受体介导了糖皮质激素发挥抗炎调节作用.该文就糖皮质激素受体在多发性肌炎/皮肌炎、系统性红斑狼疮、银屑病和白癜风等免疫相关性皮肤病发生及发展中的作用及其与糖皮质激素疗效的相关性作一综述.     

糖皮质激素受体研究进展

糖皮质激素受体包括受体α和受体β，糖皮质激素主要和糖皮质激素受体α结合，发挥其生理及药理功能，糖皮质激素受体α的密度及亲和力与糖皮质激素的疗效成正相关，糖皮质激素受体β不与糖皮质激素结合。近年来的研究表明，糖皮质激素受体β对糖皮质激素受体α的功能有拮抗作用。为此，对糖皮质激素生理及药理作用的分子生物学机制、糖皮质激素受体异常对糖皮质激素功能的影响及细胞因子、转录活化因子等对糖皮质激素受体功能的调节作用进行综述。     

糖皮质激素受体研究进展

糖皮质激素受体包括受体α和受体β,糖皮质激素主要和糖皮质激素受体α结合,发挥其生理及药理功能,糖皮质激素受体α的密度及亲和力与糖皮质激素的疗效成正相关,糖皮质激素受体β不与糖皮质激素结合。近年来的研究表明,糖皮质激素受体β对糖皮质激素受体α的功能有拮抗作用。为此,对糖皮质激素生理及药理作用的分子生物学机制、糖皮质激素受体异常对糖皮质激素功能的影响及细胞因子、转录活化因子等对糖皮质激素受体功能的调节作用进行综述。     

外用糖皮质激素治疗银屑病的疗效与糖皮质激素受体的关联

银屑病是一种常见、易复发并以角质形成细胞异常增殖及分化不全为特征的慢性炎症性皮肤病.其中外用糖皮质激素(GC)以其良好的抗炎、抗过敏及免疫抑制等作用,成为长期以来皮肤科医师治疗银屑病的重要手段之一.近年来针对银屑病的外用治疗进行了各种相关研究,发现GC与糖皮质激素受体(GR)结合并发挥抗炎作用时受到多种因素影响.该文就...     

与皮肤病相关的糖皮质激素受体的调节作用及意义

糖皮质激素(以下简称激素)的作用主要通过糖皮质激素受体介导.糖皮质激素受体的表达水平及功能状态决定着激素作用的正常发挥.激素外用制剂是炎症性皮肤病的主要治疗药物,不同个体存在对外用激素敏感程度的差异性,长期外用激素导致的副作用也限制着疗效.深入研究皮肤相关的糖皮质激素及受体作用的调节机制对于提高激素外用制剂的疗效具有重要的指导意义.     

糖皮质激素受体与狼疮肾炎治疗关系的研究

目的:检测狼疮肾炎患者外周血单个核细胞糖皮质激素受体(GR)位点数及GR mRNA的表达.方法:采用放射性配基结合位点分析法及RT-PCR方法检测38例狼疮肾炎患者GR位点数及其mRNA含量.结果:狼疮肾炎患者血中糖皮质激素和促肾上腺皮质激素与正常对照组相比,差异无统计学意义(P＞0.05),外周血单个核细胞GR位点数及其GR mRNA表达水平显著降低(P<0.01).结论:狼疮肾炎患者体内存在GR数目及转录过程的异常,可能与糖皮质激素治疗的效果不同有关.     

不同效力糖皮质激素对HaCaT细胞糖皮质激素受体调节的比较

【摘要】目的 比较三种不同的糖皮质激素对角质形成细胞的糖皮质激素受体调节效应的差异。 方法 将培养的人角质形成细胞HaCaT细胞分为空白对照组、氢化可的松作用组、地塞米松作用组、倍他米松作用组,采用反转录Real-Time PCR和Western blotting法检测各组HaCaT细胞的GRα、GRβ mRNA和蛋白质表达。 结果 三种激素均具有下调HaCaT细胞GRα表达的作用,其中氢化可的松作用最弱,而地塞米松与倍他米松作用之间无明显差异;三种激素均具有上调HaCaT细胞GRβ表达的作用,但此作用之间无明显差异。 结论 不同效力的糖皮质激素对角质形成细胞GRα和GRβ的调节效力不同,可指导临床上正确应用不同效力糖皮质激素外用制剂。     

糖皮质激素受体在白癜风患者外周血单核细胞中的表达

本研究通过检测不同类型白癜风患者外周血单核细胞中糖皮质激素受体（GCR）的表达水平,探讨其在白癜风发病中的作用。[第一段]     

Glucocorticoid receptor localization in human epidermal cells

Glucocorticoids, which are widely used in therapy, exert their immunosuppressive actions through specific receptors. These receptors have been characterized in cultured human skin fibroblasts and keratinocytes, but their localization in vitro and in vivo has not been established. To determine the tissue and cellular distribution of glucocorticoid receptors (GR), two specific polyclonal rabbit anti-human GR antibodies were used to detect these receptors in skin biopsy specimens, in freshly isolated and cultured human epidermal cells and in keratinocyte cell lines. Immunoreactive GR were only faintly detected in normal and abnormal differentiated cells and as well as those in the stratum granulosum and corneocytes. These immunolocalization studies were confirmed by fluorescence cell sorter analysis of isolated basal and suprabasal keratinocytes. Immunoreactive GR were highly expressed in normal cultured human keratinocytes, Langerhans cells and several cell lines whereas they were less expressed in melanocytes. Based upon these results the main targets of glucocorticoids in the epidermis appear to be basal and Langerhans cells. Received: 6 February 1995     

Autoimmune progesterone dermatitis: absence of contact sensitivity to glucocorticoids, oestrogen and 17-α-OH-progesterone

Autoimmune progesterone dermatitis is a rare condition, characterized by recurrent premenstrual exacerbations of a dermatosis, in which sensitivity to progesterone can be demonstrated. The sensitizing mechanism is unknown. The aim of this study was to test the hypothesis that cross-sensitivity between steroid groups could induce allergy to endogenous progesterone in these patients. 5 patients with autoimmune progesterone dermatitis and 1 with oestrogen-sensitive dermatitis have been patch tested with a corticosteroid series, conjugated oestrogen 1% in petrolatum (pet.), and 17-α-OH-progesterone 2% pet. There were no immediate or delayed reactions at 2 and 4 days to any steroid group. We have therefore been unable to demonstrate steroid cross-sensitivity, or a use for 17-α-OH-progesterone in the investigation of oestrogen - and progesterone-sensitive dermatoses.     

Topical glucocorticoids and suppression of contact sensitivity. A mouse bioassay of anti-inflammatory effects

A mouse model for assessment of the anti-inflammatory effect of topical glucocorticoids is described. Mice, sensitized to picryl chloride, had both ears painted with the sensitizer followed 2 hours later by the application of the topical steroid to one ear and the corresponding vehicle to the other. The contact sensitivity reaction, measured by swelling of the ear, was recorded 24 hours later. Dilutions of the steroid formulations inhibited the ear swelling in a manner related to dose-response. Suppression of the contact sensitivity reaction of the vehicle-treated ear as well was regarded as a systemic effect of the glucocorticoid. There seems to be a good correlation between the efficacy of the topical steroids assessed in this mouse model and the vasoconstrictor test on intact human skin.     

Glucocorticoid receptor in chick embryonic epidermis. Inhibition by progesterone of both the binding of glucocorticoid to the receptor and glucocorticoid-induced keratinization

Our previous study showed that hydrocortisone (10(-8) M) induced epidermal alpha-type keratinization in 13-day-old chick embryonic tarsometatarsal skin cultured in a chemically defined medium. In this study, we show that typical glucocorticoid receptor is present in epidermal cells of chick embryonic cultured skin and that alpha-type keratinization of epidermal cells is completely prevented by the coexistence of a 100-fold excess concentration of progesterone with glucocorticoid. The physiologic importance of the receptor is suggested by some correlation between the ability of progesterone to block both the differentiation-induction and the binding of active glucocorticoid to the receptor.     

Cushing syndrome secondary to topical glucocorticoids

An 11-year-old boy with a history of psoriasis presented with Cushingoid stigmata, which included weight gain, central obesity, violaceous striae, and facial plethora. It was discovered that he had used potent topical glucocorticoids for two months prior to the onset of his weight gain. Laboratory studies were consistent with adrenal suppression that improved after discontinuation of the use of topical glucocorticoids.     

Pulse glucocorticoids

High-dose intravenous (i.v.) methylprednisolone has been used therapeutically in a number of medical fields to avoid the complications and side effects of long-term glucocorticoid (GC) therapy and because of the perception that high-dose i.v. methylprednisolone may have "special" therapeutic effects. It is possible that aggressive early therapy with GCs allows for a more rapid taper of GCs and therefore prevents some of the dose-related side effects associated with long-term use. Some of the neurologic and rheumatologic literature related to multiple sclerosis and lupus nephritis suggest that i.v. methylprednisolone has therapeutic effects that are different from those of conventional doses of oral prednisone. There is still considerable debate about this in nondermatologic fields, and extrapolation of the role of pulse i.v. methylprednisolone to dermatologic disease, where trials are lacking, is difficult. Given this subset of possible candidates of this therapy as suggested by anecdotal reports, there is at least a rationale for considering the use of this modality in a subset of patients.