角质形成细胞生长因子与银屑病的关系

角质形成细胞生长因子是近年来发现的有着重要生物功能的生长因子,它属于成纤维细胞生长因子家族,由成纤维细胞产生。角质形成细胞生长因子可刺激角质形成细胞的增生、分化、移行,促进上皮细胞的再生、增厚,对银屑病的发病机制及其治疗可能有一定的启示。本文就角质形成细胞生长长因子和的生物学功能及其与角质形成细胞及银屑病的关系做一定综述。     

角质形成细胞和成纤维细胞对白癜风发病和治疗的影响

黑素细胞在白癜风发病及治疗中是最关键的一环,但表皮、真皮间的沟通联系对皮损及非皮损皮肤的功能均具有重要影响,其中角质形成细胞、成纤维细胞及细胞外基质等非黑素细胞起了重要作用,并影响白癜风的发病。本文从细胞因子、氧化应激等角度总结了角质形成细胞、成纤维细胞对白癜风发病的影响及在临床治疗中的作用机制。     

角质形成细胞生长因子与银屑病的关系

角质形成细胞生长因子是近年来发现的有着重要生物学功能的生长因子 ,它属于成纤维细胞生长因子家族 ,由成纤维细胞产生。角质形成细胞生长因子可刺激角质形成细胞的增生、分化、移行 ,促进上皮细胞的再生、增厚 ,对银屑病的发病机制及其治疗可能有一定的启示。本文就角质形成细胞生长因子的生物学功能及其与角质形成细胞及银屑病的关系做一综述。     

角质形成细胞生长因子对HaCaT细胞增殖的影响

目的:研究角质形成细胞生长因子(KGF)对HaCaT细胞增殖的影响,探讨KGF与银屑病表皮过度增殖的关系。方法:利用HaCaT细胞体外培养,采用KGF为增殖诱导剂,四甲基偶氮唑盐比色法(MTT)检测不同浓度的KGF对HaCaT细胞增殖率的影响;检测KGF对细胞生长曲线及细胞集落形成的影响。结果:MTT实验表明,KGF可刺激HaCaT细胞增殖,刺激作用呈浓度依赖性(r=0.981,P<0.05);10 ng/mL KGF作用下HaCaT细胞的生长速度较对照组明显加快(P<0.05),集落形成率较对照组增加(P<0.05),且细胞呈明显的增殖形态,形成的集落较大,集落内细胞多呈星状,胞内染色质丰富。结论:KGF具有显著的促HaCaT细胞增殖作用,银屑病皮损区域KGF表达增加可能是引起表皮过度增殖的重要致病因子。     

PM2.5对皮肤角质形成细胞的影响

近年来我国空气中PM2.5污染严重,皮肤是人体抵御环境污染物的重要屏障,容易受到PM2.5的损害.角质形成细胞是皮肤表皮层的主要组成细胞,在皮肤天然免疫反应中发挥着关键作用.PM2.5作用于角质形成细胞,可引发多种生物学效应.本文综述了PM2.5对皮肤角质形成细胞增殖活性、细胞凋亡、细胞自噬、芳香烃受体激活、氧化应激、...     

角质形成细胞中的信号转导

角质形成细胞是使皮肤保持稳态和参与皮肤病理生理过程的主要细胞。其增殖和分化受许多生物因子控制 ,对胞外信号反应的主要机制———蛋白磷酸化理论也在不断发展。就角质形成细胞信号转导的特点作一概述。     

角质形成细胞旁分泌作用在瘢痕疙瘩形成中的研究进展

角质形成细胞是表皮的主要组成细胞,其可分泌多种细胞因子,对临近细胞产生生物学影响。角质形成细胞旁分泌在瘢痕疙瘩的形成中发挥了一定作用,本文从角质形成细胞旁分泌在瘢痕疙瘩生物学发病机制中的作用做一综述。     

紫外线辐射对角质形成细胞产生细胞因子的影响

角质形成细胞 (包括人和小鼠正常及肿瘤细胞 )可产生多种细胞因子 ,受中波紫外线、长波紫外线及不同单色光辐射后 ,可诱导大部分细胞因子mRNA及其蛋白表达增加 ,且呈时间及剂量依赖。组胺能放大这种作用 ,而抗组胺药、糖皮质激素、非甾体抗炎药及抗氧化剂等则抑制这种作用     

紫外线辐射对角质形成细胞产生细胞因子的影响

角质形成细胞（包括人和小鼠正常及肿瘤细胞）可产生多种细胞因子，受中波紫外线、长波紫外线及不同单色光辐射后，可诱导大部分细胞因子mRNA及其蛋白表达增加，且呈时间及剂量依赖。组胺能放大这种作用，而抗组胺药、糖皮质激素、非甾体抗炎药及抗氧化剂等则抑制这种作用。     

角质形成细胞与皮肤免疫

角质形成细胞是人体表皮中的主要细胞成分,皮肤覆盖于人体表面,其意义远远超出它作为将人体内部组织和外部环境隔离开的物理屏障。皮肤还有重要的生理功能,在皮肤中存在着诸多可介导局部免疫应答的因素,包括角质形成细胞,朗格汉斯细胞,树突状Ｔ细胞和这些细胞所分泌...     

Evaluation of changes in expression pattern of oxidative stress genes under the influence of adalimumab

The psoriasis therapy consists of the inhibition of cytokines involved in inducing and development of this disease. The aim of the study was to evaluate the changes in the expression of genes related to the oxidative stress phenomenon in the culture of normal human dermal fibroblasts of Normal Human Dermal Fibroblasts (NHDF) exposed to adalimumab. NHDF culture was exposed to adalimumab for 2‐, 8‐, and 24‐hr periods. The control consisted of the same cells not exposed to adalimumab. The oligonucleotide microarrays HG‐U133A 2.0 were used to analyze the changes in gene expression in NHDF culture. Analysis showed that there are 3,881 ID mRNA involved in the induction and development of oxidative stress, the expression of which changes significantly due to the exposure of NHDF cells to adalimumab (p < .05) among 1,369 ID mRNA of them. These include genes associated with apoptosis, the p38 MAPK pathway and the PDGF pathway, and above all with pathways not yet classified. Studies have shown that two genes: NR4A2 and IL1RN, whose expression has changed the most, expressed as Fold Change (FC) seem to be the most promising molecular markers to monitor therapy and loss of cell sensitivity to treatment.     

银杏叶提取物EGb761对氧化应激下白癜风黑素细胞抗氧化作用的影响

目的:明确银杏叶提取物(EGb761)对氧化应激下白癜风黑素细胞抗氧化作用的影响。方法:人正常黑素细胞系PIG1予以H2O2处理建立氧化应激模型,予以不同浓度(50μg/m L、100μg/m L、200μg/m L、300μg/m L、400μg/m L)EGb761处理,采用MTT法检测PIG1细胞活力,生物化学方法检测脂质过氧化代谢产物丙二醛(MDA)、乳酸脱氢酶(LDH),谷胱甘肽过氧化物酶活性及含量,流式细胞仪检测细胞内活性氧(ROS)水平。结果:与模型组比较,EGb761组PIG1细胞活力、SOD、GSHPx水平增高,ROS、MDA及LDH的表达水平降低。结论:银杏叶提取物EGb761可保护黑素细胞抵抗氧化应激损伤。     

Nickel-induced keratinocyte proliferation and up-modulation of the keratinocyte growth factor receptor expression

Keratinocytes play a key role in the pathogenesis of allergic contact dermatitis (ADC) induced by the sensitizing agent nickel. We analyzed here the effects of treatment with nickel and of the pretreatment with zinc on HaCaT cells and primary human keratinocytes. Cell counting, 5-bromo-2'-deoxyuridine incorporation assay and adenosine triphosphate (ATP) bioluminescence detection showed that treatment with NiSO4 induced DNA synthesis and cell proliferation and that pretreatment with ZnSO4 was able to abrogate this proliferative effect. This nickel-induced cell growth appeared enhanced when primary human keratinocytes were co-cultured with fibroblasts. Western blot analysis demonstrated that nickel ions induced up-modulation of the expression of the keratinocyte growth factor receptors (KGFR) without affecting the keratinocyte differentiation, whereas the protein levels of the epidermal growth factor receptor (EGFR) and of its ligand transforming growth factor-alpha (TGF-alpha) appeared unmodified by the treatment. Double immunofluorescence showed that the effect of nickel on DNA synthesis was mainly exerted on KGFR expressing cells, suggesting that KGFR up-modulation could be required for the nickel-induced cell proliferation. These results indicate that KGFR and its ligands may play a role in the mechanism of action of nickel ions and in the protective effect of zinc pretreatment.     

芍药苷抗氧化应激机制研究进展

大量研究表明芍药苷具有明显的抗氧化作用,主要通过抑制氧化亢进、增强抗氧化能力、改善线粒体功能、抑制钙离子超载、抗凋亡、抑制/活化相关信号通路等多途径、多靶点发挥作用,本文将对其进行综述。     

角质形成细胞μ-阿片受体表达的研究

目的：研究不同特性的角质形成细胞μ-阿片受体的表达情况。方法：以体外培养的角质形成细胞株HaCaT细胞、人鳞状细胞癌(简称鳞癌)细胞株A431、神经母细胞瘤SK-N-SH细胞株为对象，采用逆转录(RT)-PCR方法研究细胞μ-阿片受体的表达。结果：在常规体外培养条件下，角质形成细胞株HaCaT细胞、人鳞癌细胞株A431的RT-PCR结果显示有μ-阿片受体mRNA的表达，后者的表达水平略高于前者。结论：μ-阿片受体在角质形成细胞的表达，为神经系统和皮肤通过神经肽直接发生作用提供依据。     

氧化应激下黑素细胞自噬相关基因差异表达分析

目的 探讨过氧化氢(H2O2)对黑素细胞自噬的影响及可能的调节机制.方法 取对数生长期健康人黑素细胞,分为空白对照组(不予任何处理)、阳性对照组(100 nmol/L西罗莫司处理)和实验组(体积分数为10-7～10-3的H2O2处理),处理4h后,使用CCK8法、流式细胞仪分别检测各组黑素细胞活性及凋亡率.吖啶橙染色检测自噬小泡,透射电镜下观察自噬小体,Western印迹检测自噬特异性蛋白Beclin 1、微管相关蛋白轻链3B(LC3B).最后采用包含84个自噬相关基因的RT2 Profiler PCR Array筛选自噬相关的差异表达基因.结果 黑素细胞分别经10-3、5×104、10-4、5×10-5、10-5、5×10-6、10-6H2O2处理后,细胞增殖活性及凋亡率与空白对照组相比差异均有统计学意义(F值分别为286.95、301.23,均P＜0.05),且随H2O2体积分数升高,增殖活性降低,凋亡率升高.除5×l0-6 H2O2组分别与10 5、10-6 H2O2组间相比细胞凋亡率差异无统计学意义外,上述各H2O2组间两两比较,黑素细胞增殖活性及凋亡率差异均有统计学意义(P＜0.05).吖啶橙染色及电镜观察发现,10-5 H2O2、10-6 H2O2和西罗莫司处理的黑素细胞中有自噬小体形成.Western印迹显示,10-5H2O2、10-6H2O2和西罗莫司组黑素细胞Beclin 1表达量和LC3B-Ⅱ/LC3B-Ⅰ比率均较空白对照组显著升高(P＜0.05).RT2 Profiler PCR Array结果显示,与空白对照组相比,10-5 H2O2组、10-6H2O2组和西罗莫司组中ATG12、ATG3、ULK1、PIK3CG、PTEN、PIK3C3表达均显著上调,EIF2AK3表达显著下调;10-5 H2O2组和西罗莫司组mTOR表达显著下调,ULK2表达显著上调;10-6H2O2组mTOR表达未发生明显改变,AMPK、JNK1表达显著上调.结论 体积分数为10-5和10-6的H2O2均能有效诱导黑素细胞自噬,可能与影响相关信号分子表达相关.     

Cutaneous oxidative stress

The earliest known microfossil records suggest that microorganisms existed on the earth approximately 3.8 billion years ago. Not only did sunlight drive this evolutionary process, but it also allowed photosynthetic organisms to elaborate oxygen and fundamentally change the earth’s atmosphere and subsequent evolution. Paradoxically, however, an atmosphere of 20% oxygen offers aerobic organisms both benefits and some key challenges, particularly, to the external integument. This mini‐review summarizes almost 40 years of research and provides a “60 000‐foot” perspective on cutaneous oxidative stress. Topics reviewed include the following: What are free radicals and reactive oxygen species? Where do they come from? What is their chemistry? What are their roles and/or impact on the skin? What antioxidant defenses are available to mitigate oxidative stress.     

Evaluation of nitrosative and oxidative stress in Behçet disease

Plasma nitrotyrosine and nitrite/nitrate levels as markers of nitrosative stress and plasma malondialdehyde (MDA) and protein carbonyl as markers of oxidative stress were determined in patients with Behcet disease (BD). To evaluate the balance between oxidant and antioxidant systems in these patients, we measured erythrocyte lysate CuZn superoxide dismutase (CuZn SOD) activity, plasma sulfhydryl (SH) values and total antioxidant activity. We also determined levels of plasma C-reactive protein (CRP), a key marker of inflammation, and compared them with those of healthy subjects. We found plasma nitrotyrosine levels of BD patients to be increased, indicating that nitrosative stress may occur in these patients. Plasma MDA and CRP levels in BD patients were found to be significantly higher than those in control group. However, plasma SH levels were decreased. No changes were observed in the other measured parameters of the patient group compared with the controls. These data suggest the possible involvement of nitric oxide (NO) together with reactive oxygen substances (ROS) in the pathogenesis of BD.