Review of narrowband ultraviolet B radiation in vitiligo

Vitiligo is a common, acquired pigmentary disorder of unknown etiology with great impact on patient's appearance and quality of life. It presents a therapeutic challenge to many dermatologists. Photochemotherapy using psoralen and ultraviolet A(UVA) therapy, topical and oral immunosuppresants, as well as cosmetic camouflage are also commonly employed with varying clinical efficacy. Phototherapy is a popular treatment option, which includes both of the generalized ultraviolet B(UVB) therapies, broadband UVB and narrowband UVB(NB-UVB). It has been used favorably, both alone as well as in combination with other agents like topical calcineurin inhibitors, vitamin-D analogs. Combination therapies are useful and may provide quicker regimentation and treat vitiligo with an additive mechanism of action than UVB phototherapy. Advances in technology may lead to the continuing use of UVB phototherapy as a treatment for vitiligo through the development of sophisticated devices and delivery systems as well as innovative application methods. These will provide increased therapeutic options for all vitiligo patients, particularly those with refractory disease. In this article, I have reviewed the available data pertaining to efficacy and safety issues for NB-UVB as monotherapy, its comparison with psoralen plus UVA and other modes of phototherapy, combination regimens that have been tried and future prospects of NB-UVB in vitiligo.

Hydrogen-rich saline protects against ultraviolet B radiation injury in rats

Exposure of skin to solar ultraviolet（UV） radiation induces photo-damage.Ultraviolet B（UVB） is the major component of UV radiation which induces the production of reactive oxygen species（ROS） and plays an impor-tant role in photo-damage.Hydrogen gas reduces ROS and alleviates inflammation.In this study,we sought to demonstrate that hydrogen-rich saline has the effect on skin injuries caused by UVB radiation.UVB radiation was irradiated on female C57BL/6 rats to induce skin injury.Hydrogen-rich saline and nitrogen-rich saline were ad-ministered to rats by intraperitoneal injection.Skin damage was detected by microscope after injury.UVB radia-tion had a significant affection in tumor necrosis factor alpha,interleukin（IL）-1β and IL-6 levels,tissue superox-ide dismutase,malondialdehyde and nitric oxide activity.Hydrogen-rich saline had a protective effect by altering the levels of these markers and relieved morphological skin injury.Hydrogen-rich saline protected against UVB radiation injury,possibly by reducing inflammation and oxidative stress.

Protective Effects of Jin Bai Mei Yan Prescription on Oxidative Damage and Photoaging Induced by Ultraviolet B in HaCaT Cells

Objective Ultraviolet B(UVB)mainly acts on the skin epidermis,causing oxidative damage and apoptosis of keratinocytes.Jin Bai Mei Yan Prescription(JBMYP)comprises a variety of antioxidant traditional Chinese medicines(TCM).In this study,we aimed to evaluate the effects of JBMYP on the oxidative damage induced by UVB in human immortalized epidermal keratinocytes(HaCaT)cells.Methods HaCaT cells were divided into six groups:control group,model(UVB)group,positive(UVB+vitamin E)group,UVB+JBMYP low dose group(160μg/mL),UVB+JBMYP moderate dose group(800μg/mL),and UVB+JBMYP high dose group(1600μg/mL).HaCaT cells were irradiated with UVB and treated with JBMYP for 24 h.Methyl thiazolyl tetrazolium(MTT)assay and real-time unlabeled cell function analyzer were used to assess the cell survival and proliferation rates,respectively.At the same time,the levels of intracellular reactive oxygen species(ROS),lipid peroxide malondialdehyde(MDA),glutathione(GSH),and hydroxyproline(HYP),as well as the activities of antioxidant enzyme superoxide dismutase(SOD)and catalase(CAT)were evaluated using enzyme linked immunosorbent assay(ELISA).Results Compared with the model group,the survival rate of HaCaT cells in each dosage group of JBMYP was significantly improved(P<0.05).Further,JBMYP could promote the proliferation of HaCaT cells,leading to a reduction in the contents of MDA and ROS,and increase in the contents of SOD,CAT,GSH and HYP in HaCaT cells.Conclusions JBMYP has enhanced protective effect on oxidative damage induced by UVB in HaCaT cells.

Measurement and analysis of ozone, ultraviolet B and aerosol light scattering coefficients in the Arctic

Tropospheric ozone （O3）, ultraviolet B （UVB） radiation and aerosol light scattering coefficients （SC） were investigated on a cruise ship during the fourth Chinese National Arctic Research Expedition from July 1 September 20, 2010. The results showed that O3, UVB and SC decreased with increasing latitude, with minimum values recorded in the central Arctic Ocean. Average O3 concentrations were 15.9 ppbv and 15.1 ppbv in the Bering Sea and Arctic Ocean, respectively. Ozone concentrations increased to 17.5 ppbv in the high Arctic region. Average UVB values were 0.26 W.m-2 and 0.14 W.m-2 in the Bering Sea and Arctic Ocean, respectively. The average SC in the Bering Sea was 4.3 M.m-1, more than twice the value measured in the Arctic Ocean, which had an average value of 1.7 M.m-1. Overall, UVB and SC values were stable in the central Arctic Ocean.

Influence of epigallocatechin gallate on the immune function of dendritic cells after ultraviolet B irradiation

To investigate the protective effect of epigallocatechin gallate （EGCG） on the immune function of dendritic cells （DCs） after ultraviolet B irradiation （UVB） and its underlying mechanisms, the monocytes were isolated from peripheral blood and cultivated into DCs with cytokines, such as GM-CSF and IL-4. DCs were harvested after cultivation for 7 d and subjected to irradiation with different dosages of UVB. Then, 200 μg/ml of EGCG were added in certain groups immediately after irradiation. DCs simply treated with UVB or treated with both UVB and EGCG were co-cultured with lymphocytes, and MTT assay was used to detect the ability of DCs to stimulate proliferation of lymphocytes. Surface markers CDS0, CD86, HLA-DR and CD40 were detected by flow cytometry, and the levels of IL-10 and IL-12 secreted from DCs 2d h after cultivation were measured by ELISA. It was demonstrated that UVB irradiation could inhibit the ability of DCs to stimulate the proliferation of lymphocytes and surface expressions of CDS0, CD86, HLA-DR and CD40 on DCs in a dose-dependent manner. The inhibition rate of DCs was improved to some extent after treatment with 200μg/ml of EGCG. When the concentra- tion of EGCG exceeded 100 μg/ml, the enhancing effect of EGCG on the expression of the co-stimulating molecules on DCs could be demonstrated in a dose-dependent manner. UVB showed no significant influence on the secretion of IL-10 and IL-12 from DCs, while EGCG could down-regulate the secretion level of IL-12 and up-regulate that of IL-10. It is concluded that EGCG can antagonize the inhibitory effect on DCs induced by UVB irradiation. This function has some relationship with its protecting effect of the expression of the co-stimulating molecule on the surface of DCs and the secretion level of IL-10 and IL-12.

Aggregation-induced narrowband isomeric fluorophores for ultraviolet nondoped OLEDs by engineering multiple nonbonding interactions

Traditional donor-acceptor type organic luminescent materials usually suffer from unfavorable spectral broadening and fluorescence quenching problems arising from strong inter/intra-chromophore interactions in aggregation state.Here,two ultraviolet carbazole-pyrimidine isomers(named o-DCz-Pm and m-DCz-Pm)with novel aggregation-induced narrowband phenomenon are constructed and systematic investigated by experiments and theoretical simulations.Benefitting from strengthened steric hindrance and multiple noncovalent interactions,the nonradiative decay,vibrational motion,and structural relaxation of singlet state can be effectively suppressed in aggregation state.Consequently,the electroluminescence peak of 397 nm,full width at half maximum of 21 nm and external quantum efficiency of 3.4%are achieved simultaneously in nondoped o-DCz-Pm-based device.This work paves an avenue toward the development of high-performance narrowband nondoped ultraviolet materials and organic light-emitting diodes.

The Relationship Between Ultraviolet B and DNA Methylation in Skin Cancers

Ultraviolet B is regarded as an important factor in many skin diseases,especially skin cancers.Increasingly more evidence is showing that changes in DNA methylation occur in patients with skin cancers.Changes in DNA methylation have also been observed in ultraviolet B-irradiated cells and mouse models.DNA methylation modifier enzymes are simultaneously affected.We herein review the evidence to date showing that Ultraviolet B affects changes in DNA methylation modifier enzymes in skin cancers.However,the mechanism of how ultraviolet B regulates the changes in DNA methylation modifier enzymes remains to be further elucidated.Understanding the mechanism by which ultraviolet B modulates DNA methylation modifier enzymes can help to identify potential therapeutic markers or targets and develop novel strategies for preventing or treating ultraviolet B-induced skin damage.

Peripheral carbazole units-decorated MR emitter containing B−N covalent bond for highly efficient green OLEDs with low roll-off

Boron−nitrogen doped multiple resonance(BN-MR)emitters,characterized by B−N covalent bonds,offer distinctive advantages as pivotal building blocks for facile access to novel MR emitters featuring narrowband spectra and high efficiency.However,there remains a scarcity of exploration concerning synthetic methods and structural derivations to expand the library of novel BN-MR emitters.Herein,we present the synthesis of a BN-MR emitter,tCz[B−N]N,through a one-pot borylation reaction directed by the amine group,achieving an impressive yield of 94%.The emitter is decorated by incorporating two 3,6-di-tbutylcarbazole(tCz)units into a B−N covalent bond doped BN-MR parent molecule via para-C−π−D and para-N−π−D conjugations.This peripheral decoration strategy enhances the reverse intersystem crossing process and shifts the emission band towards the pure green region,peaking at 526 nm with a narrowband full-width at half maximum(FWHM)of 41 nm.Consequently,organic light emitting diodes(OLEDs)employing this emitter achieved a maximum external quantum efficiency(EQEmax)value of 27.7%,with minimal efficiency roll-off.Even at a practical luminance of 1000 cd·m^(−2),the device maintains a high EQE value of 24.6%.

Effect of Ultraviolet Radiation on Hsp70 Protein Expression in HaCaT Cells

Ultraviolet radiation by its wavelength is divided into: UVA, UVB and UVC. Only UVA and UVB manage to penetrate the ozone layer, but due to anthropological activities, all of them are capable of interacting with humans to a greater or lesser extent, and can generate adverse effects such as cellular stress when interacting with intra-and extracellular biomolecules. The skin is the first organ in contact with UV radiation, and the stress it generates can be analyzed by the expression of a bioindicator of cellular damage such as Hsp70. Therefore, the objective of the project was: to determine the effect of UVA, UVB and UVC radiation on HaCaT epithelial cells, by analyzing the expression of Hsp70. Materials and methods: HaCaT cells were cultured in vitro, which were irradiated with UVA, UVB and UVC light at different doses, to subsequently determine the degree of Hsp70 expression by Immunodetection by PAGE-SDS and Western Blot. Results: Basal expression of Hsp70 was observed in no irradiated HaCaT cells. When HaCaT cells were irradiated with UVA, UVB, UVC, an increase in this Hsp70 protein was observed. With UVA, a higher degree of expression was observed at a time of 30 minutes of irradiation. With UVB the highest expression shifted to a time of 20 minutes. With UVC, overexpression was observed after 10 minutes. Conclusion: UV radiation generates cellular stress on HaCaT cells, evaluated by the stress bioindicator Hsp70. According to the wavelength of UV radiation, those that have a shorter wavelength have a greater potential for cellular damage, such as UVC.

2%超分子水杨酸对UVB所致小鼠光老化损伤的修复研究

目的 探究2%超分子水杨酸对中波紫外线(UVB)所致小鼠光老化损伤的修复作用。方法 选择30只6~8周龄昆明雌鼠,随机分为空白对照组、UVB组、UVB+2%超分子水杨酸组,各10只。空白对照组小鼠正常日光照射饲养, UVB组、UVB+2%超分子水杨酸组隔日用UVB照射1次,辐照12周,其中UVB+2%超分子水杨酸组小鼠在UVB照射后涂抹1次2%超分子水杨酸,非照射日每日涂抹1次;最后1次辐照结束后48 h观察三组小鼠皮肤组织形态变化情况,应用苏木精-伊红(HE)染色观察小鼠背部皮肤显微结构改变情况,测定表皮、真皮厚度,应用Masson染色观察真皮胶原纤维排列情况,测定胶原纤维含量,用免疫组化染色观察皮肤组织p21、p53表达情况。比较三组小鼠背部皮肤外形情况、皮肤显微结构改变情况及皮肤组织p21、p53阳性表达情况。结果 与空白对照组相比,UVB组小鼠皮肤粗糙,有深皱纹毛孔扩大,缺乏弹性,皮肤呈褐黄色斑,皮革样外观,镜下见毛细血管扩张,结痂,为典型光老化特征;UVB+2%超分子水杨酸组皮肤外观有隐约褐色斑,镜下见皮肤有散在、不规则褐色斑片,光老化症状较轻。三组背部皮肤损伤程度比较有明显差异性(P<0.05);UVB组背部皮肤损伤程度明显大于空白对照组和UVB+2%超分子水杨酸组,有明显差异性(P<0.05);空白对照组与UVB+2%超分子水杨酸组皮损程度比较也有明显差异性(P<0.05)。空白对照组表皮厚度、真皮厚度、真皮胶原纤维含量分别为(18.55±1.80)μm、(350.08±35.16)μm、(0.46±0.05)OD, UVB组分别为(79.68±21.37)μm、(611.62±16.37)μm、(0.15±0.30)OD, UVB+2%超分子水杨酸组分别为(60.99±11.49)μm、(467.94±20.71)μm、(0.32±0.03)OD。三组表皮厚度、真皮厚度及真皮胶原纤维含量比较有明显差异性(P<0.05);UVB+2%超分子水杨酸组和UVB组表皮厚度、真皮厚度明显多于空白对照组,真皮胶原纤维含量显著少于空白对照组,有明显差异性(P<0.05);UVB+2%超分子水杨酸组表皮厚度、真皮厚度明显少于UVB组,真皮胶原纤维含量多于UVB组,有明显差异性(P<0.05)。免疫组化显示空白对照组未见有p21、p53阳性表达。UVB+2%超分子水杨酸组皮肤组织p21、p53阳性表达率分别为30.00%、10.00%,低于UVB组的80.00%、60.00%,有明显差异性(P<0.05)。结论 2%超分子水杨酸对UVB所致小鼠光老化皮肤有修护保护作用,其机制与抑制凋亡相关基因p21、p53表达有关。

真空紫外协同Co^(2+)催化过硫酸氢钾降解罗丹明B

有机染料具有毒性强、色度高、不易降解等特性,为了高效去除有机染料,实验以真空紫外(VUV)为光源,研究了VUV协同Co^(2+)催化过硫酸氢钾(PMS)降解典型有机染料罗丹明B(RhB)的反应机制和转化途径.结果表明:①在RhB初始浓度为80 mg/L,Co^(2+)和PMS投加量分别为15μmol/L、0.5 mmol/L的条件下,VUV/Co^(2+)/PMS体系反应10 min,RhB去除率可达99.1%.VUV/Co^(2+)/PMS体系对RhB降解遵循一级动力学规律,反应速率常数(k)随初始质量浓度的增加而减小.②溶液初始pH对反应速率有较大的影响,随着pH减小,反应速率也同时减小.投加量为30 mmol/L的HCO_(3)^(−)、Cl^(−)均表现出显著的抑制作用,相较于对照组,RhB去除率由99.1%分别降至66.0%、84.2%,而NO_(3)^(−)和SO_(4)^(2−)抑制作用不显著;印染助剂柠檬酸钠也会显著抑制RhB降解.③自由基捕获实验和电子顺磁共振(EPR)测试结果表明,VUV/Co^(2+)/PMS体系中存在的氧化物种包括硫酸根自由基(SO_(4)^(−)·)、羟基自由基(·OH)、单线态氧(1O2).④根据紫外可见吸收光谱和质谱结果,初步推断RhB分子降解主要通过活性氧(ROS)攻击造成共轭结构破坏和N-位脱乙基等作用.另外,对总有机碳(TOC)进行测试,30 min时RhB矿化度可达到43.8%.研究显示,VUV/Co^(2+)/PMS体系能够有效去除RhB.

丹参素对UVB诱导的皮肤光老化小鼠的保护作用和抗氧化机制研究

研究丹参素(DSS)对紫外线B(UVB)诱导的皮肤光老化(SP)小鼠的保护作用和抗氧化机制。建立了UVB诱导的SP小鼠模型,使用3个剂量的DSS(20,40和80 mg/(kg·d))治疗小鼠8周,结束后分别测定了各组小鼠的表皮含水量。通过HE染色评价皮肤组织形态,Masson三色染色评价胶原蛋白沉积。按照试剂盒说明测定皮肤组织中氧化应激指标(SOD、CAT、GSH-Px和MDA)和炎症指标(TNF-α和IL-6)水平。通过RT-qPCT和Western blotting检测了皮肤组织中MMP-1、Collagen I、Nrf2、Keap1、HO-1、NF-κB p65和p-NF-κB p65的mRNA或蛋白水平。结果显示,DSS剂量依赖性地提高了UVB诱导的SP小鼠表皮含水量,减轻皮肤损伤,促进胶原形成(P<0.05)。DSS抑制了UVB诱导的SP小鼠皮肤组织中MMP-1的转录和表达,促进了Collagen的转录和表达(P<0.05)。DSS升高了UVB诱导的SP小鼠皮肤组织中SOD、CAT和GSH-Px的水平,降低了MDA的水平(P<0.05)。DSS降低了UVB诱导的SP小鼠皮肤组织中TNF-α和IL-6的水平(P<0.05)。DSS促进了UVB诱导的SP小鼠皮肤组织中Nrf2和HO-1的转录和表达,抑制了Keap1的转录和表达(P<0.05)。DSS抑制了UVB诱导的SP小鼠皮肤组织中p-NF-κB p65的表达(P<0.05)。本研究表明DSS可有效改善UVB诱导的小鼠SP,其机制与Nrf2和NF-κB信号通路有关。

6-巯基-5-三唑并[4,3-b]-s-四嗪(MTT)的密度泛函理论研究

采用密度泛函理论(Density functional theory,DFT),在B3LYP/6-31g(d)(C,H,N,S),Ag原子采用LanL2d赝势基组水平上对甲醛(HCHO)与4-氨基-5肼基-3-巯基-1,2,4-三唑(4-amino-5-hydrazino-3-mercapto-1,2,4-triazole,AHMT)衍生化反应生的成产物6-巯基-5-三唑并[4,3-b]-s-四嗪(6-mercapto-5-triazolo[4,3-b]-s-tetrazine,MTT)及其银配合物进行结构优化,优化结果表明MTT的结构是一个近平面结构.通过对频率计算,获得MTT分子及其银配合物的拉曼光谱,对400-1800 cm^(-1)波段内的拉曼光谱特征峰进行了指认.同时讨论了MTT分子的表面静电势,分析可能发生化学反应的位点.并采用含时密度泛函理论(Time Dependent density functional theory,TDDFT)对MTT分子与Ag3配合物的激发态进行了计算分析,并使用电荷转移光谱对Ag配合物与MTT之间电荷转移关系进行了研究.该研究对MTT分子的光谱测定和电子性质提供了理论基础.

The Action of Aloe Anthraquinones in Protecting the Growth of Soybean from Ultraviolet Radiation Stress

In order to investigate the protective effect of aloe anthraquinones on growth and development of soybean against ultraviolet B radiation stress from the morphological structure and physio-chemical indices. The results showed that, stressed by the enhanced ultraviolet b radiation, the soybean gave a dwarfed plant, shrunken leaf area and decreased photosynthetic pigment, while an ascended MDA content. Spraying aloe anthraquinones effectively relieved the reductions of chloro- phyll content and biomass and decreased the production of MDA under the radia- tion of UV-B. Moreover, under the UV-B radiation, waxy substances on epidermal cells increased remarkably and the stomas showed obvious subsidence, while spraying aloe anthraquinones could maintain the structure and shape of cells similar to that under natural light, and the stomas subsidence as well.

大黄酸通过抑制p38 MAPK磷酸化减轻UVB诱导的皮肤光老化损伤

揭示大黄酸(rhein)对紫外线B(UVB)诱导的皮肤光老化损伤的影响及机制。将大鼠分为6组,分别为正常对照组(NC)、UVB组、低剂量Rhein组(L-Rhein)、中剂量Rhein组(M-Rhein)、高剂量Rhein组(H-Rhein)和高剂量Rhein+p38 MAPK激动剂Anisomycin组(H-Rhein+Anisomycin)。NC组大鼠仅剃毛,不照射,其他组进行UVB照射。大黄酸的给药途径为口服。大鼠共治疗8周。治疗结束后,分别测定各组大鼠的体重、表皮含水量、皮肤组织中氧化应激指标水平,并对皮肤组织进行HE染色和Masson三色染色,计算胶原体积分数(CVF)。通过RT-qPCR检测皮肤组织中TNF-α、IL-1β、IL-6、MMP-1、MMP-3和CollagenⅠmRNA水平。通过Western blotting检测皮肤组织中p-p38 MAPK和p38MAPK蛋白水平。结果显示,与UVB组比较,L-Rhein组、M-Rhein组和H-Rhein组大鼠皮肤p38 MAPK磷酸化水平降低,表皮含水量升高,皮肤损伤减轻,CVF升高,皮肤MMP-1和MMP-3 mRNA相对表达量降低,CollagenⅠmRNA相对表达量升高,皮肤SOD、CAT和GSH-Px水平升高,MDA水平降低,皮肤TNF-α、IL-1β和IL-6 mRNA相对表达量降低(P<0.05)。Anisomycin减弱了大黄酸的皮肤保护作用(P<0.05)。说明大黄酸通过抑制p38 MAPK磷酸化减轻UVB诱导的皮肤光老化损伤。因此,大黄酸可能是一种防治皮肤光老化的候选天然药物。

增强UV-B胁迫对小麦幼苗CaM含量的影响

[目的]对增强UV-B胁迫下小麦幼苗中钙调素(CaM)含量进行研究,进而研究增强UV-B胁迫下小麦幼苗体内Ca^(2+)-CaM通路的情况。[方法]采用二次盐析、Sephadex G-50凝胶过滤层析等方法,从小麦幼苗中分离纯化的CaM,并采用PDE法测定CaM含量。[结果]增强UV-B胁迫导致小麦幼苗CaM含量增加了23%,这可能为增强UV-B胁迫导致钙离子增多,进而调控CaM所致。[结论]结果为小麦抗辐射机制的研究奠定了一定的基础。

CO_(2)点阵激光联合NB-UVB治疗非节段型白癜风的效果及对心身状态的影响

目的 探讨CO_(2)点阵激光联合窄谱中波紫外线(NB-UVB)治疗非节段型白癜风(NSV)的效果及对心身状态的影响。方法 选取2022年1月至2023年1月徐州市矿务集团总医院皮肤科门诊治疗的70例NSV患者,采用随机数表分为NB-UVB组(n=35,NB-UVB治疗)和联合组(n=35,CO_(2)点阵激光联合NB-UVB治疗)。比较两组临床疗效,白癜风面积及严重程度(VASI)评分,肿瘤坏死因子(TNF-α)、γ-干扰素(IFN-γ)和白细胞介素-4(IL-4)水平,T淋巴细胞亚群(CD4^(+)、CD8^(+)、CD4^(+)/CD8^(+))水平,以及临床症状自评量表(SCL-90)评分。结果 联合组总有效率高于NB-UVB组,差异有统计学意义(P<0.05)。治疗后,联合组VASI、SCL-90评分以及TNF-α、IFN-γ、CD8^(+)水平低于NB-UVB组,差异有统计学意义(P<0.05);且联合组IL-4、CD4^(+)、CD4^(+)/CD8^(+)水平高于NB-UVB组,差异有统计学意义(P<0.05)。结论 CO_(2)点阵激光联合NB-UVB治疗NSV的效果显著,能抑制炎症反应,调节免疫平衡,改善心身状态。

Increased 5-hydroxymethylcytosine and Ten-eleven Translocation Protein Expression in Ultraviolet B-irradiated HaCaT Cells

Background： DNA hydroxymethylation refers to a chemical modification process in which 5-methylcytosine （5mC） is catalyzed to 5-hydroxymethylcytosine （5hmC） by ten-eleven translocation （TET） family proteins. Recent studies have revealed that aberrant TETs expression or 5hmC level may play important roles in the occurrence and development of various pathological and physiological processes including cancer and aging. This study aimed to explore the relation between aberrant DNA hydroxymethylation with skin photoaging and to investigate the levels of TETs, 5mC, and 5hmC expression 24 h after 40 mJ/cm^2 and 80 mJ/cm^2 doses of ultraviolet B （UVB） irradiation to HaCaT cells. Methods： To explore whether aberrant DNA hydroxymethylation is also related to skin photoaging, 40 mJ/cm^2 and 80 mJ/cm^2 doses of UVB were chosen to treat keratinocytes （HaCaT cells）. After 24 h of UVB irradiation, 5mC and 5hmC levels were determined by immunohistochemistry （IHC） and immunofluorescence （IF）, and at the same time, the expression levels of matrix metalloproteinase 1 （MMP-1） and TETs were assessed by reverse transcription-polymerase chain reaction or Western blot analysis. Results： After 40 mJ/cm^2 and 80 mJ/cm^2 doses of UVB exposure, both IHC and IF results showed that 5hmC levels increased significantly, while the 5mC levels did not exhibit significant changes in HaCaT cells, compared with HaCat cells without UVB exposure. Moreover, compared with HaCat cells without UVB exposure, the levels ofTET1, TET2, and TET3 mRNA and protein expression were significantly upregulated （mRNA： P = 0.0022 and 0.0043 for TET1; all P 〈 0.0001 for TET2; all P = 0.0006 for TET3; protein： P = 0.0012 and 0.0006 tbr TET 1 ; all P = 0.0022 for TET2; and all P = 0.0002 for TET3）, and the levels of MMP- 1 mRNA expression increased dose dependently in 40 mJ/cm^2 and 80 mJ/cm^2 UVB-irradiated groups. Conclusion： UVB radiation could cause increased 5hmC and TET expression, which might become a novel biomarker in UVB-related skin aging.

Receptor interacting protein 1 involved in ultraviolet B induced NIH3T3 cell apoptosis through expression of matrix metalloproteinases and reactive oxygen species production

Background Receptor interacting protein 1 （RIP1）, which plays a key role in apoptosis, cell survival and programmed cell necrosis, is one of the most important proteins in the RIP family. The purpose of this study was to investigate the roles of RIP1 in the apoptosis, the generation of reactive oxygen species （ROS） and the expression of matrix metalloproteinases （MMPs） induced by ultraviolet B （UVB） in fibroblasts. Methods siRNA targeting RIP1 was used to silence RIP1 expression in the NIH3T3 fibroblasts. The mRNA and protein levels of MMP-1 and MMP-3, caspase-3 and -8 activities, and ROS activities were determined by reverse transcriptasequantitative polymerase chain reaction （RT-qPCR）, immunoblotting, caspase activity assay, immunofiuorescence, and flow cytometry. Results The mRNA and protein expressions of MMP-1 and MMP-3 were significantly increased in RIP1 deficient NIH3T3 cells at 24 hours after UVB treatment. At 24 hours after exposure to UVB, RIP1 deficient NIH3T3 cells presented apoptotic morphology, and the apoptosis rate was significantly increased accompanied by pronounced increase in caspase-8 and -3 activities. ROS production was inhibited by UVB at 12 hours in RIP1 deficient NIH3T3 cells. Conclusion RIP1 is involved in NIH3T3 cell damage induced by UVB via participating in the apoptosis, expression of MMPs and ROS production.

Protective effect of sulfated polysaccharides from a Celluclast-assisted extract of Hizikia fusiforme against ultraviolet B-induced photoaging in vitro in human keratinocytes and in vivo in zebrafish

Our previous study evaluated the in vitro and in vivo antioxidant activities of sulfated polysaccharides from a Celluclastassistedextract of Hizikia fusiforme (HFPS). The results indicate that HFPS possesses potent antioxidant activity and suggestthe potential use of HFPS to combat photoaging. In this study, we investigated the ultraviolet (UV) protective effect of HFPSin vitro in keratinocytes (HaCaT cells) and in vivo in zebrafish. The results indicate that HFPS significantly reduced thelevel of intracellular reactive oxygen species (ROS) and improved the viability of UVB-irradiated HaCaT cells. In addition,HFPS remarkably decreased apoptosis formation in UVB-irradiated HaCaT cells in a dose-dependent manner. The in vivotest results also demonstrate that HFPS significantly reduced intracellular ROS levels, cell death, NO production, and lipidperoxidation levels in UVB-irradiated zebrafish in a dose-dependent manner. These results suggest that HFPS possessesstrong in vitro and in vivo UV-protective effects, making it a potential ingredient in the cosmeceutical industry.