黄芩素对氧化应激状态下白癜风黑素细胞线粒体超微结构和功能的影响

目的:明确黄芩素对氧化应激状态下白癜风黑素细胞(PIG3V)线粒体超微结构和功能的影响。方法:常规培养白癜风黑素细胞系PIG3V细胞,分为空白对照组、黄芩素组、H_2O_2组及黄芩素+H_2O_2组。电镜观察线粒体超微结构;MTT法检测线粒体活性;流式细胞术检测线粒体膜电位;荧光素酶报告系统检测细胞ATP含量;RT-PCR检测线粒体DNA拷贝数。结果:与H_2O_2组比较,黄芩素+H_2O_2组线粒体结构损害轻,线粒体活性率、膜电位、ATP含量及DNA拷贝数高。结论:黄芩素减轻氧化应激状态下白癜风黑素细胞线粒体结构和功能损害,增强细胞抗氧化能力。     

氧化应激与白癜风的相关性研究

白癜风是一种临床常见的色素脱失性皮肤病.病因及发病机制复杂,近年来关于氧化应激与白癜风发病的关系成为白癜风研究的热点之一,本文就氧化应激与白癜风发病及病情活动的相关性进行分析.     

白癜风的抗氧化治疗

近年来氧化应激被认为是白癜风发病与病情发展的重要机制,因而抗氧化治疗白癜风成为研究热点,部分抗氧化治疗药物已经应用于临床治疗并取得满意效果,本文将对抗氧化治疗药物做一综述,为今后抗氧化相关研究及治疗提供参考。     

白癜风氧化应激机制及抗氧化治疗进展

白癜风是一种常见的色素脱失性疾病,临床上以表皮黑素细胞破坏缺失而出现色素脱失斑为主要特征.其发病机制不明.近年来发现,通过体内外各种因素,引起白癜风患者体内的氧化-抗氧化系统平衡失调,导致体内的活性氧簇或活性氮簇增加,引起氧化应激,造成黑素细胞损伤.随着研究的深入,一些人工或天然抗氧化剂应用于白癜风的临床治疗,如槲皮素、胎盘制剂、银杏叶提取液等.     

过氧化氢对培养白癜风黑素细胞超微结构的影响

目的 探讨白癜风黑素细胞对外源性氧化剂的敏感性及氧化应激在白癜风发病中的作用.方法 以0.5mmol/L过氧化氢分别处理4例白癜风患者外观正常皮肤及6例正常对照皮肤培养的黑素细胞,采用透射电镜观察细胞的形态学变化,并应用图像分析技术和形态计量学方法,测定线粒体、粗面内质网及黑素小体的超微结构变化.结果 0.5mmol/L过氧化氢对正常人黑素细胞形态学及主要细胞器超微结构无明显影响.过氧化氢处理后的白癜风黑素细胞线粒体、内质网分别与处理前及正常对照处理后比较,数量明显减少,差异均有统计学意义(P<0.01).线粒体局部空化,内质网扩张.部分黑素小体体积显著增大,但黑素小体数量与过氧化氢处理前及正常对照处理后比较,差异无统计学意义(P>0.05).结论 过氧化氢可能通过破坏细胞的能量代谢和蛋白合成系统,使黑素细胞功能逐渐减退,促使白癜风的发生.     

白癜风氧化应激发病机制的研究进展

白癜风发病机制复杂,涉及遗传、免疫、氧化应激、功能性黑素细胞凋亡和（或）丢失、神经体液等假说。本文将对Keap1/Nrf2/ARE信号转导通路与氧化应激进行综述。     

NB-UVB对白癜风患者黑素细胞生物学特性的影响

目的：明确窄谱中波紫外线(narrow-band UVB, NB-UVB)对白癜风患者的黑素细胞生物学特性的影响。方法：提取34例白癜风患者皮损处黑素细胞进行体外培养。每例样本分组后分别接受不同的照射剂量（0、20、40、60、80、100 mJ/cm2）的NB-UVB处理，照射后1 d采用免疫印迹法对黑素细胞中微管相关蛋白轻链3 II/I(LC3 II/I)、酸化哺乳动物雷帕霉素靶蛋白(p-mTOR)、自噬信号磷酸化磷酸腺苷蛋白激酶(p-AMPK)、P26蛋白的表达情况进行测定。照射后2d、3d、4d采用MTT法对黑素细胞的增殖活性进行测定，采用NaOH染色法对黑素细胞中黑素含量进行测定。结果：随着NB-UVB照射剂量的增加,LC3 II/I和p-AMPK表达水平逐渐上调，p-mTOR和P26的表达水平逐渐下降。不同NB-UVB剂量下，黑素细胞增殖水平增加，但随剂量的增加，增殖的程度逐渐减弱。不同NB-UVB剂量黑素细胞中黑素水平升高，且呈剂量依赖式递增。结论：NB-UVB能够有效调节白癜风患者黑素细胞自噬相关蛋白表达水平，活化自噬信号通路，促进黑素细胞增殖及黑素合成能力。     

白癜风相关的黑素细胞抗原

自身免疫在白癜风发病机理中占重要地位。患者血清中存在抗黑素细胞自身抗体 ,通过与黑素细胞抗原结合 ,引发一系列免疫反应 ,破坏黑素细胞。现已明确的白癜风相关黑素细胞抗原分为胞浆抗原和胞膜抗原两大类 ,这些抗原通过多种途径共同作用 ,介导了白癜风的免疫病理过程。     

中药的抗氧化作用治疗白癜风研究进展

白癜风是一种以皮肤出现大小形态不等的白色斑片、边缘清楚为特征的后天获得的色素脱失性皮肤病,黑素细胞的功能障碍或缺失,使皮肤和黏膜色素产生减少或消失.近年来对白癜风发病机制的多项研究证明,氧化应激可能是白癜风发生发展的一个重要因素.     

白癜风免疫微环境对黑素细胞CXCL10表达的影响

目的:明确白癜风免疫微环境对黑素细胞CXCL10表达的影响。方法:采用qRT-PCR检测进展期白癜风患者皮损组织中的细胞因子;采用qRT-PCR及ELISA检测白癜风免疫微环境中上调的细胞因子对黑素细胞系PIG1 CXCL10表达和分泌。结果:进展期白癜风患者皮损组织中IFN-γ、TNF-α和IL-1βmRNA表达上调;三者联合刺激显著上调PIG1细胞CXCL10 mRNA的表达以及蛋白分泌,并呈现时间依赖性。结论:白癜风局部免疫微环境促进黑素细胞表达及分泌CXCL10,可能参与白癜风发病。     

Role of oxidative stress and autoimmunity in onset and progression of vitiligo

Vitiligo is an acquired depigmentation disorder characterized by the loss of functional melanocytes from the epidermis. Two major theories of vitiligo pathogenesis include autoimmunity and oxidative stress‐mediated toxicity in melanocytes. The present study aimed to evaluate both the hypotheses in vitiligo patients and to investigate their role in the disease onset and progression. Antimelanocyte antibody levels and lipid peroxidation (LPO) levels were evaluated in 427 patients and 440 controls; antithyroid peroxidase (TPO) antibody levels were estimated in 102 patients and 72 controls. Patients showed a significant increase in LPO and antimelanocyte antibody levels compared to controls. Antimelanocyte antibody and LPO levels were higher in active vitiligo compared to stable. Only 9.8% of patients showed the presence of anti‐TPO antibodies in their circulation. Oxidative stress may be the initial triggering event to precipitate vitiligo in Gujarat population, which is exacerbated by contributing autoimmune factors together with oxidative stress.     

Increased sensitivity of melanocytes to oxidative stress and abnormal expression of tyrosinase-related protein in vitiligo

BACKGROUND: Vitiligo is a depigmenting disease of the skin, which may derive from programmed melanocyte death or destruction due to inherent sensitivity to oxidative stress arising from either toxic intermediates of melanin, a melanocyte-specific protein, or other sources. Tyrosinase-related protein (TRP) -1 has been shown to be involved not only in melanin biosynthesis but also in the prevention of premature melanocyte death in animals. OBJECTIVES: To clarify the biological role of human TRP-1 in melanocyte survival. METHODS: Cultured melanocyte strains from an active advancing border of vitiligo were established and studied. RESULTS: The established 'vitiligo melanocytes' showed large perikaryon and stubby dendrites. They showed early cell death when exposed to oxidative stress (ultraviolet B) and increased and abnormal immunostaining and immunoprecipitation by antibodies against human and mouse TRP-1, indicating an altered synthesis and processing of TRP-1. In pulse-chase and sequential immunoprecipitation experiments, vitiligo melanocytes revealed abnormal protein-protein interaction with calnexin, a melanogenesis-associated chaperone, suggesting altered folding and maturation of nascent TRP-1 polypeptides. Northern blot analysis indicated a decreased expression of TRP-1 mRNA, but heteroduplex analysis and verification of the mutation at the carboxy terminus of TRP-1 by restriction enzyme analysis did not show any abnormality. CONCLUSIONS: Our study suggests that the early cell death of vitiligo melanocytes is related to their increased sensitivity to oxidative stress, which may arise from complex processes of abnormal synthesis and processing of TRP-1 and its interaction with calnexin.     

白癜风发病过程研究进展

白癜风是皮肤科常见的色素脱失性疾病,其发病机制目前尚不明确,主要有遗传、氧化应激、黑素细胞丢失、免疫等学说,其发病可能经历了始动阶段、效应阶段及致病阶段,本文对其进行了综述。     

喜树果浸膏搽剂治疗白癜风临床研究

目的探讨喜树碱外用制剂对白癜风的临床疗效。方法应用我院自行研制的喜树果浸膏搽剂(喜树果浸膏二甲基亚砜溶液)，治疗白癜风患者81例，男31例，女50例。年龄1．3—65岁。病程为1周到30年。分布于头部、颈部、躯干、四肢的单发及多发形皮损。局部涂搽，一日二次。结果用药后最快一周出现色素沉着，14天白斑消退，平均3-4周恢复色素。治愈62例，好转17例，无效2例，总有效率97．4％。对其中54例治愈者随访一年局部无复发，随访率87．9％。结论喜树果浸膏搽剂治疗白癜风疗效好，显效快，安全可靠，方便，我们认为喜树碱浸膏制剂有促进色素细胞增殖，移行及促进色素生成的作用，但其确切机理有待进一步研究。     

Mini-epidemic of contact dermatitis from ginkgo tree fruit (Ginkgo biloba L.)

3 cases of contact dermatitis from ginkgo fruit are reported. Swelling of the prepuce can be the only clinical sign of intolerance, as was observed in 1 case. Diagnosis of contact dermatitis to ginkgo fruit should be made in cities where female ginkgo trees grow, in Chinese, Japanese and South-East Asian subjects, who are aware of the ginkgo nut's culinary qualities within the fruit, as well as in children who play with the fallen fruits as "marbles".     

Vitiligo: interplay between oxidative stress and immune system

Vitiligo is a multifactorial polygenic disorder with a complex pathogenesis, linked with both genetic and non‐genetic factors. The precise modus operandi for vitiligo pathogenesis has remained elusive. Theories regarding loss of melanocytes are based on autoimmune, cytotoxic, oxidant–antioxidant and neural mechanisms. Reactive oxygen species (ROS) in excess have been documented in active vitiligo skin. Numerous proteins in addition to tyrosinase are affected. It is possible that oxidative stress is one among the main principal causes of vitiligo. However, there also exists ample evidence for altered immunological processes in vitiligo, particularly in chronic and progressive conditions. Both innate and adaptive arms of the immune system appear to be involved as a primary event or as a secondary promotive consequence. There is speculation on the interplay, if any, between ROS and the immune system in the pathogenesis of vitiligo. The article focuses on the scientific evidences linking oxidative stress and immune system to vitiligo pathogenesis giving credence to a convergent terminal pathway of oxidative stress–autoimmunity‐mediated melanocyte loss.     

The effects of EGb 761 on lipid peroxide levels and superoxide dismutase activity in sunburn

BACKGROUND/PURPOSE: Free oxygen radicals are involved in inflammatory skin reactions induced by ultraviolet B (UVB). In this study, the effect of a herbal antioxidant Ginkgo biloba extract (EGb 761) was investigated in UVB irradiated mice skin. METHODS: The study was carried out on four groups of mice (n = 6 in each group). The first group was a control group (G1). The second group (G2) was only exposed to acute UVB irradiation. The third group (G3) received 100 mg/kg/day of EGb 761 orally for 5 days before UVB irradiation and the fourth group (G4) was given only a single dose of EGb 761 immediately after UVB irradiation. Eighteen hours after exposing to UVB, lipid peroxide levels, and superoxide dismutase (SOD) activities were studied and UVB damage was evaluated histopathologically according to "sun-burn cell count". RESULTS: The SOD activities and Malondialdehyde (MDA) levels in G2, G3 and G4 were found to be decreased significantly when compared with G1 (P < 0.05). The SOD activities of G3 and G4 were higher when compared with G2 (P < 0.05). The number of sunburn cells (SBCs) was the highest in G2. CONCLUSIONS: Our results suggest that EGb 761 may have an important effect, both as a protective and therapeutic agent, in sunburn after UVB irradiation.