姜黄素抑制小鼠生殖器官氧化产物生成的研究

目的:探讨姜黄素对氧化应激小鼠子宫、卵巢组织脂质过氧化水平的影响。方法:昆明种雌性成年小鼠40只,随机分成正常对照组,0 mg/kg Cur组,100 mg/kg Cur组,200 mg/kg Cur组,连续用药21天,实验结束后测定小鼠子宫、卵巢组织以及血清中丙二醛(MDA)、活性氧(ROS)的含量。结果:100 mg/kg Cur组,200 mg/kg Cur组血清、子宫以及卵巢氧化应激产物ROS、MDA与砷暴露组相比均有降低,具有明显统计学差异(P0.05)。结论 :姜黄素可降低小鼠子宫、卵巢组织以及血清中氧化产物MDA、ROS的含量,对小鼠卵巢氧化应激引起的生殖器官损伤有保护作用。     

何首乌治疗雄激素性脱发的分子机制：基于生物信息学和分子对接方法

 目的 揭示何首乌治疗雄激素性脱发的分子机制并提供潜在的药物靶点。方法 使用中医药分子机制生物信息学数据库和5个疾病基因数据库建立何首乌有效成分-雄激素性脱发靶点网络和蛋白互作网络，依据拓扑学分析进行核心子网络筛选，并进行GO和KEGG富集分析。对连接度最高的10个基因做分子对接。结果 根据何首乌有效成分和疾病潜在靶点交集得到1 357个共同靶基因。经拓扑学分析最终筛选得到由67个基因组成的核心子网络。KEGG富集结果显示何首乌主要通过调节炎症反应、细胞凋亡、氧化应激、自噬等通路发挥生物学功能。分子对接显示PIK3CA-大黄素、PIK3CA-大黄酚、PIK3CA-扁蓄苷和PIK3CB-大黄素结合能均<-9 kcal/mol。结论 何首乌治疗雄激素性脱发的机制可能通过大黄素介导PI3K/Akt通路调控PIK3CA和PIK3CB的表达来调控细胞凋亡。此外还涉及抑制炎症反应、氧化应激以及诱导黑色素生成等过程。     

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。     

莫诺苯宗联合维甲酸对C57BL/6小鼠及SCF转基因小鼠模拟白癜风的作用

目的 探讨比较莫诺苯宗联合维甲酸局部应用诱导C57BL/6及SCF转基因小鼠产生白癜风样表型的作用，构建组织病理学相似度高、脱色效果持久稳定的白癜风样小鼠模型，为白癜风基础研究选择动物模型提供依据。方法 分别将C57B L/6小鼠和SCF转基因鼠各15只随机分为三组：对照组(Control)、莫诺苯宗组(MBEH)、莫诺苯宗+维甲酸联合组(MBEH+RA),使用40%莫诺苯宗单独或40%莫诺苯宗联合0.1%维甲酸涂搽30 d, 3 d 1次，对照组除备皮外不进行任何处理。应用免疫荧光、免疫组化等方法观察黑素细胞、CD8⁺T细胞、NK细胞、黑色素颗粒和氧化应激水平等指标的变化。结果 与莫诺苯宗组相比，联合组可快速诱发两种小鼠皮肤脱色。与正常对照组相比，联合组小鼠皮肤脱色部位黑素细胞及黑色素含量均显著减少，可见较多CD8⁺T细胞及NK细胞浸润，局部氧化应激水平升高。结论 莫诺苯宗联合维甲酸可在两种不同类型的小鼠中快速诱导白癜风样表型，应用表皮含有黑素细胞的SCF转基因小鼠造模更适用于白癜风的相关研究。     

大疱及疱疹性皮肤病

20141403氧化应激与天疱疮（综述）/胡静（泸州医学院）,李灵//中国皮肤性病学杂志.-2014,28（4）.-418～420 天疱疮是一种累及皮肤和黏膜的危重的表皮内大疱性皮肤病,是自身免疫性疾病的典型。病因尚不完全清楚,现在有很多与天疱疮发病机制相关的假说,但每种假说都不能完整解释天疱疮的发病原因。目前,氧化应激在天疱疮中的作用越来越受到关注。文中从天疱疮中存在氧化应激及氧化应激参与天疱疮的发病机制方面进行了综述。参19     

氧化应激与皮肤病相关性的研究进展

皮肤微环境中氧化应激和抗氧化的平衡失调是皮肤疾病发生、发展的重要基础。紫外线已成为引起皮肤氧化应激损伤的越来越主要的原因。本文综述了氧化应激尤其是紫外线产生的氧化应激损伤与临床上常见皮肤疾病发生、发展的相关性。     

氧化应激与荨麻疹关系的系统综述

目的 运用系统综述方法综合评价氧化应激与荨麻疹(Urticaria)的关系,为荨麻疹发病机制探讨及合理有效诊治提供理论依据。方法 按照制定的检索策略,计算机检索PubMed、Embase、中国知网(CNKI)、中国维普数据库(VIP)和万方数据库(WanFang),查找有关氧化应激与荨麻疹关系的病例-对照研究,检索时限均从建库至2018年10月。由2名研究者按照纳入与排除标准独立进行文献筛选、资料提取和质量评价,并进行描述性分析。结果 共纳入文献9篇,因文献同质性较差,不符合Meta分析条件,因此采用定性的系统综述分析方法。结果显示:①与对照组相比,非甾体类消炎药(NSAIDs)诱导的荨麻疹中,血浆(CuZn/SOD)和红细胞(CuZn/SOD、GSH-Px和CAT)中酶活性差异无统计学意义,血浆和红细胞中丙二醛的含量间差异无统计学意义。②急、慢性荨麻疹(包含不同形式的物理性荨麻疹)中氧化应激指标与疾病活动性呈正相关。结论 除NSAIDs诱导的荨麻疹外,氧化应激参与荨麻疹的发病过程,且氧化应激程度与患者病程及病情相关。     

病毒感染患者的氧化应激状态的研究

近年来发现人体疾病的发生、发展与机体的氧化应激状态密切相关 ,病毒感染的机体常处于慢性氧化应激状态。病毒诱导宿主细胞产生氧化应激 ,释放大量活性氧自由基 ,在活性氧自由基的作用下病毒复制增强 ,应用抗氧化剂治疗病毒性疾病已取得初步疗效。总结目前关于氧化应激与病毒感染的研究 ,从脱氧核糖核酸病毒、核糖核酸病毒及逆转录酶病毒 3方面阐述病毒感染患者的氧化应激状态 ,旨在为病毒性疾病的治疗探寻新的途径     

病毒感染患者的氧化应激状态的研究

近年来发现人体疾病的发生、发展与机体的氧化应激状态密切相关，病毒感染的机体常处于慢性氧化应激状态。病毒诱导宿主细胞产生氧化应激，释放大量活性氧自由基，在活性氧自由基的作用下病毒复制增强，应用抗氧化剂治疗病毒性疾病已取得初步疗效。总结目前关于氧化应激与病毒感染的研究，从脱氧核糖核酸病毒、核糖核酸病毒及逆转录酶病毒3方面阐述病毒感染患者的氧化应激状态，旨在为病毒性疾病的治疗探寻新的途径。     

中西医治疗卵巢氧化应激的进展

随着生活节奏的不断加快、心理压力的不断增大、人们生活习惯及饮食结构的改变,不孕症的患病因素日趋复杂,卵巢氧化应激引起的不孕症也逐年增长。本文旨在对国内外近些年有关治疗卵巢氧化应激的研究进行阐述,为更好的治疗卵巢氧化应激、改善人类生殖功能提供一定的理论依据。     

Proceedings of the 3rd Annual Meeting of the Japanese Photoaging Research Society, Kobe, Japan, 23 August 2002

The nematode Caenorhabditis elegans has proven a robust genetic model for studies of aging and the roles of stress. In this review we focus on the genetics of select long‐lived and short‐lived mutants of C. elegans that have proven useful in revealing the relationships that exist between oxidative stress and life span. The former are known to be controlled by an insulin/insulin‐like signaling pathway, while the latter are affected by mitochondrial functions.     

Determination of the antioxidant capacity of an antioxidant combination using the fluoroscan assay in vitro and visualization of its effects using histological methods

The effects of a well-defined combination of antioxidants on oxidative stress were investigated in vitro using classical techniques together and its protective effects against UV damage were investigated using a newly developed skin model. After determining the cytotoxic potential of the combination, its quenching effect on the oxidative stress induced by hydrogen peroxide was quantified by a nonfluorescent (C-H2DCF-DA/AM)/fluorescent (C-DCF) dye system using the fluoroscan assay. Two different skin models consisting of normal human skin fibroblasts and the keratinocyte cell line HaCaT were developed and subsequently used to visualize the protective effects of the combination against UVA damage. No evidence of any cytotoxic potential of the combination could be seen. Supplementation of human skin fibroblasts demonstrated a clear, dose-dependent enhancement of the antioxidative capacity of these cells. Histological findings confirmed the beneficial effects of the antioxidants present in the combination in the skin models used. Supplementation induced morphological changes leading to a thicker epidermal layer providing evidence of the positive effects of the treatment on the viability of the keratinocytes after UVA irradiation. This in vitro study provided convincing evidence of the combined antioxidative action of -tocopherol, -carotene, tomato extract, grape seed extract, ascorbic acid and selenium yeast, and indicated a potential beneficial action of the combination against oxidative stress caused by external oxidative stress factors such as UV irradiation.     

Astragaloside IV attenuates high glucose-induced human keratinocytes injury via TGF-β/Smad signaling pathway

ObjectivesIn this study, we have investigated the effect of Astragaloside IV on keratinocytes’ proliferation, migration, oxidative stress, apoptosis, inflammation, and relevant signaling pathway, using human keratinocytes exposed to high glucose.BackgroundAstragaloside IV is one of the main active ingredients of Astragalus membranaceus (Fisch.) Bunge. Previous studies have found that Astragaloside IV exerts positive effects in various disease models and promotes wound healing.MethodsCell proliferation and migration of keratinocytes, oxidative stress indicators, cell apoptosis rate, inflammatory factors, and key proteins in the TGF-β/Smad signaling pathway were evaluated by molecular biology/biochemical techniques, fluorescence microscope, and flow cytometry.ResultsHigh glucose inhibited the cell proliferation and migration of keratinocytes, upregulated the levels of MDA, ROS, IL-6, IL-8, and Smad7, and decreased the levels of SOD, IL-10, TGF-β1, p-Smad2, and p-Smad3. Astragaloside IV attenuated the dysfunction of keratinocytes, oxidative stress, cell apoptosis, and inflammation, but activated TGF-β/Smad signaling pathway. Meanwhile, the addition of SB431542 (the inhibitor of TGF-β/Smad signaling pathway) eliminated the impact of Astragaloside IV on high glucose-induced keratinocytes.ConclusionsThese results strongly suggest that Astragaloside IV may be a potential drug candidate for accelerating diabetic wound healing, by protecting keratinocytes against damages induced by high glucose and TGF-β/Smad pathway is involved in this process at the cellular level.     

Pseudoxanthoma elasticum: oxidative stress and antioxidant diet in a mouse model (Abcc6-/-)

Pseudoxanthoma elasticum (PXE), a multisystem disorder characterized by ectopic mineralization of soft connective tissues, is caused by mutations in the ABCC6 gene. The pathomechanistic details of the mineralization process are largely unknown, but oxidative stress has been suggested to play a role. In this study, we tested Abcc6(-/-) mice, which serve as a model of PXE, for markers of the oxidative stress in the liver and serum. The total antioxidant capacity as well as markers of protein oxidation and lipid peroxidation suggested the presence of chronic oxidative stress. Feeding these mice for 5 months with a diet supplemented with antioxidants (vitamins C and E, selenium, and N-acetylcysteine) countered the oxidative stress but did not modify the ectopic mineralization process. These results suggest that the Abcc6(-/-) mice suffer from chronic oxidative stress but this does not contribute to connective tissue mineralization, the hallmark of PXE.     

Nrf2/ARE在抗光老化中的作用及机制研究进展

光老化是皮肤长期暴露于紫外线,引起的慢性损伤。既往研究表明氧化应激是造成皮肤急慢性炎症的主要原因,甚至引起细胞突变,以致肿瘤的形成,而紫外线的照射是引起氧化应激主要原因之一。当紫外线照射下产生过多的活性氧(reactive oxygen species,ROS),超过机体清除能力,可影响相关信号通路传导,导致光老化和癌变。最近的研究提示NF-E2相关因子2(NF-E2 related factor2,Nrf2)是参与细胞氧化应激反应的关键因子,通过结合下游的抗氧化反应元件(antioxidant response element,ARE)在细胞防御保护中发挥重要作用,能有效抵御紫外线照射引起的皮肤损伤。该文就Nrf2/ARE在抗光老化中的作用及相关机制的研究作一综述。     

Idebenone: a new antioxidant - Part I. Relative assessment of oxidative stress protection capacity compared to commonly known antioxidants

Topical applications of skin care products containing antioxidants have become increasingly popular. Numerous studies have elucidated the biological effects of these substances. General antiaging effects, anti-inflammatory properties, photoprotective properties, and prevention of ultraviolet (UV) immunosuppression have been documented. However, a standardized method to characterize and compare the properties and oxidative stress protection capacity of antioxidants was lacking. A multistep in vitro process utilizing a variety of biochemical and cell biological methods combined with in vivo studies was designed to compare the oxidative stress protective capacity of commonly used antioxidants. Data were presented for L-ascorbic acid, dl-alpha-tocopherol, kinetin, dl-alpha lipoic acid, ubiquinone, and idebenone. Methods included using UV-induced radical trapping/scavenging capacity measured by photochemiluminescence, pro-oxidative systems (LDL-CuSO(4), microsome-NADPH/ADP/Fe(3+)) with measurement of primary and secondary oxidation products, UVB irradiation of human keratinocytes, and in vivo evaluation, using the human sunburn cell (SBC) assay. Correlation and trends between in vitro and in vivo results were established, and the standardized test protocol was used to quantify oxidative stress protection capacity of antioxidants. Summarizing and totaling the data equally weighted for each oxidative stress study, the overall oxidative protection capacity scores of 95, 80, 68, 55, 52, and 41 were obtained for idebenone, dl-alpha tocopherol, kinetin, ubiquinone, L-ascorbic acid, and dl-alpha lipoic acid, respectively. The higher the score, the more effective the overall oxidative stress protection capacity of the antioxidant became. This multistep protocol may serve as a standard in investigating and comparing new putative antioxidants for topical use as well as a valuable tool to assess the anti-inflammatory properties, photoprotective properties, and prevention of UV immunosuppression of topical antioxidants.     

Protective role of AQP3 in UVA-induced NHSFs apoptosis via Bcl2 up-regulation

Aquaporin-3 (AQP3), a water/glycerol-transporting protein that facilitates water, urea, and glycerol transport, can inhibit arsenite-induced apoptosis by up-regulating Bcl-2. However, whether it has a protective role in ultraviolet A (UVA)-induced apoptosis in normal human skin fibroblasts is not known. In this study, we demonstrate that mild UVA treatment fails to induce oxidative cell stress and apoptosis in normal human skin fibroblasts (NHSFs) overexpressing AQP3. After severe UVA irradiation, there was an increase in oxidative cell stress and apoptosis when AQP3 levels decreased. We also found that silencing AQP3 sensitized NHSFs to low-dose UVA. Overexpressing AQP3 was protective against high-dose UVA-induced oxidative stress and apoptosis. Besides, we observed that Bcl-2 may be involved in UVA-induced apoptosis. Our findings suggested that the water/glycerol-transporting protein AQP3 plays a role in resistance to UVA-induced apoptosis.