不同染色法检测豚鼠皮肤黑色素的比较研究

[目的]用几种组织化学染色方法来探讨豚鼠皮肤黑色素反应,对不同染色法进行比较。[方法]利用多巴氧化酶法(DopA)、硫酸亚铁吸收法、亚铁氰化钾法和银浸染色法(Masson-fontana)对黑色素细胞进行染色。[结果]多巴氧化酶法,黑色素细胞呈黑色。硫酸亚铁吸收法,黑色素细胞和嗜银细胞呈暗绿色。亚铁氰化钾法,黑色素细胞和嗜银颗粒为蓝黑色。银浸染色法,黑色素细胞、亲银细胞和嗜铬细胞均呈黑色。[结论]多巴氧化酶法在几种方法中是最适合观察黑色素细胞数量和黑色素颗粒的方法。     

自体黑色素细胞培养移植治疗白癜风的临床疗效研究

目的 观察自体黑色素细胞培养移植治疗肢端型白癜风的临床疗效,并分析影响疗效的相关因素.方法 选择肢端型白癜风患者62例(共96处皮损),根据治疗方法分为窄谱中波紫外线治疗组(A组)50处和自体黑色素细胞培养移植治疗组(B组)46处,比较两组的临床疗效.计算黑色素细胞分裂时间.结果 B组有效率显著高于A组[71.7％(33/46)比36.0％ (18/50),P＜0.05];自体黑色素细胞培养移植治疗的临床疗效与患者的年龄、皮损部位和病程无显著相关性(P＞0.05),与黑色素细胞分裂时间有显著相关性(P＜0.05).结论 自体黑色素细胞培养移植是治疗肢端型白癜风的有效方法,黑色素细胞分裂时间是影响其疗效的主要因素.     

自体黑色素细胞培养移植治疗30例白癜风的效果分析

目的:探讨自体黑色素细胞培养移植治疗30例白癜风的效果。方法:将60例肢端型白癜风病人平均分为研究组与对照组。对照组应用窄谱中波紫外线进行治疗,研究组应用自体黑色素细胞培养移植治疗。结果:研究组治疗的总有效率为72.92%,明显高于对照组的36.73%(P<0.05)。结论:黑色素细胞培养移植治疗肢端型白癜风疗效显著,值得临床推广与应用。     

低水平氚相对生物效应的实验研究：黑色素细胞的分化异常

以小鼠皮肤黑色素细胞异常分化为指标，观察了低水平对＾６０Ｃｏｒ射线的相对生物产应，结果表明，氚剂量为０．１Ｇｙ时，ＲＢＥ为２．１６，并比较了一次与分次腹腔注入相同剂量氚水对黑色素细胞异常分化的影响，结果分次照射轻于一次照射。     

一种新的皮肤黑色素细胞及肥大细胞缺乏的小鼠模型

目的 分析Kit基因突变的W-4Bao白斑小鼠的表型特征.方法 遗传试验观察突变小鼠的大体表型,多巴染色法观察黑色素细胞,甲苯胺蓝染色法观察肥大细胞.结果 突变基因杂合子小鼠腹部三角形白斑,肢端、尾端白化;皮肤组织内黑色素细胞及肥大细胞无明显差异.突变纯合子小鼠全身被毛白色,眼周、耳廓、背部局部被毛末端灰黑色,黑眼;皮肤组织内多巴阳性黑色素细胞、肥大细胞较对照组明显减少几近完全缺失.结论 Kit基因错义突变不仅导致了W-4Bao杂合子及纯合子小鼠黑色素细胞缺乏,同时影响了肥大细胞的发育.     

以致癌物诱导小鼠皮肤产生活性黑色素细胞:一种检测皮肤致癌物的新方法

迄今已有不少观察,证明化学致癌物可诱导皮肤黑色素母细胞(melanoblasts)的黑色素形成(melanogenesis)。因此,提出黑色素细胞激活作用(melanocyte activation)可用作为检测化学致癌物的方法之一。为进一步对这种测试系统作出评价,本研究应用多种强致癌物,弱致癌物,肿瘤促进剂,以及非致癌物质对有色素成年小鼠内毛囊表皮(interfollicular epidermis)黑色素细胞的作用。     

低水平氚相对生物效应的实验研究－黑色素细胞的分化异常

以小鼠皮肤黑色素细胞异常分化为指标，观察了低水平氚对￣（６０）Ｃｏγ射线的相对生物效应（ＲＢＥ），结果表明，氚剂量为０．１Ｇｙ时，ＲＢＥ为２．１６，并比较了一次与分次腹腔注入相同剂量氚水对黑色素细胞异常分化的影响，结果分次照射轻于一次照射。     

信息速递

自体皮肤黑色素细胞移植治疗白癜风白癜风的病因至今尚未完全阐明,其治疗更是医学上的难题之一患者虽然无生理上的痛楚,但心理上的痛苦难以言表解放军北京空军总医院皮肤科和临床实验科协作, 开展自体皮肤黑色素细胞移植治疗白癜风已成功地为     

祛斑增白当心汞中毒

美容化妆品已成为众多女性的一种时尚,但美白仍是世界性难题。目前还没有一种添加剂,能让人安全快速达到美白目的。真正祛斑的产品成分是熊果苷、维生素C等,其作用只能是较慢地逐步改变肤质。汞被称为“黑色素细胞的毒药”,它能杀死黑色素细胞,有短期内迅     

果蔬不是美容的万能药

水果控们注意啦!好吃抗氧化、美容美白消水肿……这些是不是你疯狂吃水果的理由?为了能美丽,一次一斤樱桃二斤木瓜可不是天方夜谭,以果蔬代替正餐屡见不鲜。到底应不应该?※问题1:据说富含VC的果蔬能美白祛斑?回答:黑色素细胞位于皮肤表面与真皮层基底细胞层之间。每当受到紫外线、遗传、疾病、内分泌、药物甚至辐射的影响,便会产生黑色素,让皮肤变深并沉积成斑点。维生素C有助于皮肤再生,在帮助胶原蛋白生长外,与维生素E结     

烟酰胺对人皮肤黑素细胞黑素转运作用研究

目的 研究烟酰胺作用于人皮肤黑素细胞后,对黑素细胞中钙信号、细胞骨架的影响及其与黑素小体运动速率和分布的作用,并探讨其中的相互关系.方法 体外培养的人皮肤黑素细胞中分别加入0.00、0.05、0.25、1.25、6.25 mg/ml烟酰胺后,用荧光抗体染色法检测黑素细胞中游离钙离子浓度,以生化法测定细胞中钙泵活性,以Western Blot蛋白浓度测定法测定动力蛋白Dynein的表达水平,显微镜下观察活细胞中烟酰胺对黑素小体运动速率及黑素小体分布的影响.结果 烟酰胺对人皮肤黑素细胞中游离钙浓度影响显著,并有剂量.效应关系,y=76.4612-5.435x(r=0.97);细胞钙泵活性随烟酰胺浓度的增加而下降;细胞中动力蛋白表达随烟酰胺加入的浓度不同而改变;在烟酰胺浓度为0.05和25 mg/ml时,细胞功能正常的情况下,钙泵活性正常,能够调控细胞中的物质转运,而黑素细胞中Dynein表达却明显减少(P<0.05),而烟酰胺浓度为1.25mg/ml时,钙泵活性减弱(P<0.05),黑素细胞中动力蛋白Dynein的表达增加(P＜0.05).当烟酰胺作用浓度为0.25和1.25 mg/ml时,黑素细胞中黑素小体的运动速率明显增加(P<0.05),同时细胞中黑素小体密集度随烟酰胺浓度增加而下降.结论 烟酰胺参与黑素的转运过程并能加快黑素细胞中黑素小体的运动速率,显示烟酰胺对钙泵、细胞动力蛋白Dynein表达和黑素小体运动具有调控作用,作用浓度为一重要调节因素.

Abstract：

Objective To study the effects of nicotinamide on the human skin melanocytes and try to explore the potential mechanism of nicotinamide on the calcium signal transduction.cytoskeleton.Methods The primary cultured human skin melanocytes from foreskin were selected as the target cells in the present study.0.00,0.05,0.25,1.25 and 6.25 mg/ml nicotinamide were applied respectively.Western blot,fluorescent probes(Flu-3AM),flow cytometry analysis and time-lampse microscope digital skill were used to evaluate the effects of nicotinamide on melanosome motility and the melanosome distribution in melanocytes.Results The results showed that nicotinamide had a potential effect on regulating free calcium concentration in a dose-dependent manner(y=76.461 2-5.435x,r=0.97);The activity of Na~+-K~+-Ca~(2+)-ATPase was down regulated with the increasing concentration of nicotinamide.The expression of cellular dyrnein was also altered by nicotinamide;Na~+-K~+-Ca(2+)-ATPase activity was kept normal when given 0.05,0.25 mg/ml nicotinamide,while the dynein protein expression was inhibited(P＜0.05),Na~+-K~+-ca~(2+)-ATPase activity was decreased significantly when given 1.25 mg/nicotinamide(P<0.05),while the dynein protein expression was increascd (P<0.05).When treated with 0.25 mg/ml and 1.25 mg/concentration of nicotinamide,movement velocity in melanocytes was accelerated and the distribution characters of melanosomes were different among groups.Conclusion Nicotinamide may mediate the melanin transport in melanocytes in vitro.The concentration of nicotinamide plays a key role in the melanin regnladng path.Nicotinamide could be used as a regulator for melanin transport.     

Hypothesis: possible role for the melatonin receptor in vitiligo: discussion paper.

A new unifying hypothesis for the aetiology of vitiligo is proposed, in which we postulate that the final destruction of melanocytes in vitiligo results from a cascade of reactions initiated by a disregulation of melanogenesis, caused by activation of the melatonin receptor. These events result in the high and uncontrolled production of free radicals and toxic products of melanogenesis which sequentially damage or destroy melanocytes and keratinocytes, provoke an autoimmune response against exposed intracellular or altered cell surface antigens, and increase the propensity of melanocytes to undergo malignant transformation.     

Beta-carotene uptake and bioconversion to retinol differ between human melanocytes and keratinocytes.

beta-Carotene is one of the carotenoids that has been considered to play a role in the natural defense against ultraviolet-induced skin cancer. It is not known whether epidermal cells are able to accumulate beta-carotene and, subsequently, convert it to vitamin A. We used normal cultured human keratinocytes and melanocytes to study the uptake, and possible bioconversion to retinol, of authentic or [14C]beta-carotene. The uptake was much higher in melanocytes than in keratinocytes, corresponding to a fivefold difference in the intracellular fraction after two days of incubation. An increased level of cellular retinol was noted after one day of beta-carotene incubation. The conversion of [14C]beta-carotene to [14C]retinol peaked at 24 hours of incubation in keratinocytes and melanocytes. The results suggest that beta-carotene can function as a local supply of vitamin A in the skin and that melanocytes are especially likely to store beta-carotene.     

UVA与UVB对人体黑素细胞生长的影响

[目的]探讨长波紫外线（UVA）和中波紫外线（UVB）照射人体黑素细胞作用的差异。[方法]以不同剂量UVA和UVB分别照射黑素细胞,用四甲基偶氮唑盐微量酶反应比色法（MTT）测量细胞增殖率,比色法测定酪氨酸酶活性,吸光度测定黑素含量的变化。[结果]人体黑素细胞经0-2．25J／cm^2UVA照射后,黑素含量和酪氨酸酶活性无明显改变,其中较高剂量UVA（〉1．8J／cm^2）可使黑素细胞存活率下降。0-0．06J／cm^2UVB能明显抑制黑素细胞存活率,并能激活酪氨酸酶和促进黑素细胞的黑素合成。[结论]离体水平UVB对黑素细胞的促黑素合成作用明显强于UVA。     

Inhibitory effects of progestogens on the estrogen stimulation of melanocytes in vitro

Background

The use of oral estrogen-progestogen contraceptives may cause melasma, an epidermal hyperpigmentation in sun-exposed areas of the face. It is assumed that elevated estrogen levels lead to the activation of melanocytes, while the role of the gestagen component of contraceptives in pigmentation remains unclear and may vary between the different progestogens. In this study, we analyzed the distinct effects of progesterone and chlormadinone acetate (CMA) on melanocytes in comparison with estrogen.

Study Design

Human melanocytes were exposed to different concentrations of 17β-estradiol and progestogens and analyzed for proliferation by a fluorometric cell viability assay and for pigmentation by a ³H-labeled tyrosine assay. Subgroups of cells were additionally irradiated with UVA or UVB.

Results

Proliferation of melanocytes was induced by 17β-estradiol (0.1 and 1 nM) in approximately half of the experiments, while progesterone (100 nM) and CMA (100 nM) reduced the proliferation rate by 38% and 27%, respectively. The pigmentation activity was slightly stimulated by 17β-estradiol, whereas progestogens had no effect on the tyrosinase activity.

Conclusions

Our data suggest that progesterone and CMA can inhibit proliferation of human melanocytes, which counteracts the stimulatory effects of estrogen. This may be of relevance for the choice of progestogen in oral contraceptives to prevent the development of melasma.     

日本刺参胶原肽对B16黑素瘤细胞黑素合成的影响

目的:研究不同分子量日本刺参胶原肽A1(6000U相似文献   

Environmental estrogens alter early development in Xenopus laevis

A growing number of environmental toxicants found in pesticides, herbicides, and industrial solvents are believed to have deleterious effects on development by disrupting hormone-sensitive processes. We exposed Xenopus laevis embryos at early gastrula to the commonly encountered environmental estrogens nonylphenol, octylphenol, and methoxychlor, the antiandrogen, p,p-DDE, or the synthetic androgen, 17 alpha-methyltestosterone at concentrations ranging from 10 nM to 10 microM and examined them at tailbud stages (approximately 48 hr of treatment). Exposure to the three environmental estrogens, as well as to the natural estrogen 17 beta-estradiol, increased mortality, induced morphologic deformations, increased apoptosis, and altered the deposition and differentiation of neural crest-derived melanocytes in tailbud stage embryos. Although neural crest-derived melanocytes were markedly altered in embryos treated with estrogenic toxicants, expression of the early neural crest maker Xslug, a factor that regulates both the induction and subsequent migration of neural crest cells, was not affected, suggesting that the disruption induced by these compounds with respect to melanocyte development may occur at later stages of their differentiation. Co-incubation of embryos with the pure antiestrogen ICI 182,780 blocked the ability of nonylphenol to induce abnormalities in body shape and in melanocyte differentiation but did not block the effects of methoxychlor. Our data indicate not only that acute exposure to these environmental estrogens induces deleterious effects on early vertebrate development but also that different environmental estrogens may alter the fate of a specific cell type via different mechanisms. Finally, our data suggest that the differentiation of neural crest-derived melanocytes may be particularly sensitive to the disruptive actions of these ubiquitous chemical contaminants.     

Monozygotic twins with congenital guttate leukoderma

We report here two cases of congenital guttate hypomelanotic macules observed in monozygotic twins. They both have had discrete leukoderma regions in the axillae, inguinal region and lower abdomen since birth. The size and the shape did not change until at least the age of nine. Development of both patients was otherwise normal. The split-DOPA reaction revealed no DOPA-positive melanocytes in the hypomelanotic skin, but electron microscopy revealed melanocytes that were regular but decreased in number. Cytogenetic analysis of the peripheral leukocytes revealed normal female karyotype in both cases. Considering the unique pattern of the leukoderma lesions which occurred in both monozygotic twins, this might be a new clinical entity.     

烟酰胺对长波紫外线照射黑素细胞黑素合成的干预

目的研究烟酰胺对长波紫外线（UVA）致人皮肤黑素细胞黑素合成的干预作用。方法观察0．2J／cm^2 UVA（365nm）照射人皮肤黑素细胞后，烟酰胺在不同剂量时对人皮肤黑素细胞中黑素合成和转运的干预作用。结果0．2J／cm^2 UVA照射后，黑素细胞中黑素含量明显增加，UVA照射后的人皮肤黑素细胞给予不同剂量的烟酰胺时，黑素细胞中黑素含量明显下降，10．0mmol／ml时作用更为明显。烟酰胺在有效抑制黑素含量的同时，对黑素细胞的细胞周期、细胞凋亡及DNA指数无明显影响；0．2J／cm^2 UVA照射后立即给予烟酰胺时，烟酰胺可以调节黑素细胞中mRNA的表达水平。结论烟酰胺能够拮抗UVA的致黑作用；10．0mmol／ml烟酰胺在干预UVA所致的黑素细胞致黑作用的同时，对黑素细胞的作用浓度是安全的；烟酰胺参与其中黑素的转运；鉴于烟酰胺拮抗UVA致黑作用的有效结果，烟酰胺有望用于防护UVA照射所引起的晒黑作用。     

Cytotoxicity and antiproliferative activities of several phenolic compounds against three melanocytes cell lines: relationship between structure and activity

Polyphenolic compounds are widely distributed in the vegetable kingdom and are therefore consumed regularly in the human diet. Epidemiological studies suggest that foods rich in polyphenolic compounds contribute to reducing the risk of cancer. The purpose of our work is to: 1) study the possible cytotoxicity and antiproliferative effects of 13 polyphenolic compounds on 3 cell lines of melanocytes, 2 of melanoma (B16F10 and SK-MEL-1), and 1 of nontransformed melanocytes (Melan-a); and 2) identify the possible relationship between the chemical structure of the tested compounds and their effect on cellular viability. The said polyphenolic compounds corresponded to 8 flavonoids with varying hydroxyl and methoxyl substituents, related structurally through the oxidation state of their flavonoid skeleton, a catechin polymer and 4 phenolic acids. The cytotoxic activity of all the studied compounds was modest or not apparent. The flavonoids luteolin, tangeretin, baicalein, quercetin, and myricetin, and gallic acid showed antiproliferative effects on the tested lines. Our results suggest that a correlation exists between the structural oxidation state and the position, number, and nature of substituents of the polyphenolic compounds studied and their antiproliferative effects.