Guinea Pig Model of Cataract induced by Ultraviolet Ray Irradiation

Guinea pig model of cataract was obtained by ultraviolet ray irradiation on both eyes of 47 guinea pigs for 6-8 months. Seven eye-lenses irradiated by ultraviolet ray selected randomly for optical micro-scopic and electron microscopic examinations revealed typical pathological findings such as obvious swelling and widening of gaps of the lens fibres.

Investigation of bystander effect in Molt-4 cells induced by ultraviolet ray

Objective： To find out whether ultraviolet ray, a kind of non-ionic ray, could cause the bystander effect, the UV exposed MOLT-4 cells had been investigated. Methods： Two experiment groups were carried out, in which cells were culture and treated at two concentrations： 2 × 10^5/mL and 5 × 10^5/mL. All other treatments were the same. Part of the cells was labeled with DID and exposed to UV ray for 40 s as effect cells; other cells was untreated as bystander cells. Then, the cells were co-cultured and harvested at 4 h interval over a period of 24 h. Annexin V-FITC/PI assay was used to evaluate the bystander effect in bystander cells co-cultured with effected cells. Laser confocal microscope method was used to observe the morphologic changes of the bystander cells. Results： The percentage of cells undergoing apoptosis in the bystander cells was increased over time compared with the control group. They were 6.84%, 8.09%, 9.88%, 17.64%, 17.43%, 30.99% and 37.93% respectively in 0 h, 4 h, 8 h, 12 h, 16 h, 20 h and 24 h. When observed by laser scanning confocal microscope, the bystander cells show some classic character of apoptosis such as chromosome condense, phosphatidylsedne transfer and formation of apoptotic bodies. Conclusion： Bystander effect is significant in un-irradiated bystander MOLT-4 cells when co-cultured with UV exposed cells.

Protective effect of Peroxiredoxin 6 (PRDX6) treatment on the rat model with corneal injury caused by ultraviolet ray

Objective: To study the protective effect of Peroxiredoxin 6 (PRDX6) treatment on the rat model with corneal injury caused by ultraviolet ray. Methods: SD male rats were selected as experimental animals and randomly divided into control group, model group and PRDX6 group, corneal injury models were established by UV irradiation, and they received PRDX6 intervention. The contents of oxidative stress molecules, apoptosis molecules and MMPs/TIMPs in corneal tissues were detected on the 12 d after intervention. Results: MDA, AOPP, Fas, FasL, Bax, Caspase-3, MMP2 and MMP9 contents in corneal tissue of model group were significantly higher than those of control group while T-AOC, SOD, GSH-Px, Bcl-2, Survivin, XIAP, TIMP1 and TIMP2 contents were significantly lower than those of control group;MDA, AOPP, Fas, FasL, Bax, Caspase-3, MMP2 and MMP9 contents in corneal tissue of PRDX6 group were significantly lower than those of model group while T-AOC, SOD, GSH-Px, Bcl-2, Survivin, XIAP, TIMP1 and TIMP2 contents were significantly higher than those of model group. Conclusion: PRDX6 has inhibitory effect on the oxidative stress and apoptosis in corneal injury process caused by ultraviolet ray.

The Association of Socioeconomic Status with the Burden of Cataract-related Blindness and the Effect of Ultraviolet Radiation Exposure: An Ecological Study

Objective To assess the association of socioeconomic status with the burden of cataract blindness in terms of year lived with disability(YLD) rates and to determine whether ultraviolet radiation(UVR) levels modify the effect of socioeconomic status on this health burden.Methods National and subnational age-standardized YLD rates associated with cataract-related blindness were derived from the Global Burden of Disease(GBD) study 2017. The human development index(HDI) from the Human Development Report was used as a measure of socioeconomic status.Estimated ground-level UVR exposure was obtained from the Ozone Monitoring Instrument(OMI)dataset of the National Aeronautics and Space Administration(NASA).Results Across 185 countries, socioeconomic status was inversely associated with the burden of cataract blindness. Countries with a very high HDI had an 84% lower age-standardized YLD rate [95%confidence interval(CI): 60%–93%, P < 0.001] than countries with a low HDI;for high-HDI countries, the proportion was 76%(95% CI: 53%–88%, P < 0.001), and for medium-HDI countries, the proportion was48%(95% CI: 15%–68%, P = 0.010;P for trend < 0.001). The interaction analysis showed that UVR exposure played an interactive role in the association between socioeconomic status and cataract blindness burden(P value for interaction = 0.047).Conclusion Long-term high-UVR exposure amplifies the association of poor socioeconomic status with the burden of cataract-related blindness. The findings emphasize the need for strengthening UVR exposure protection interventions in developing countries with high-UVR exposure.

The Polypeptide in Chlamys farreri can protect human dermal fibroblasts from ultraviolet B damage

To investigate the effect of polypeptide from Chlamys farreri (PCF) on NHDF in vitro, we modeled oxidative damage on normal human dermal fibroblasts (NHDF) exposed to ultraviolet B (UVB). In this study, 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydro-genase (LDH) were tested to measure cell viability. Enzymes including superoxide dismutase (SOD), glu-tathione peroxidase (GSH-PX), catalase (CAT) and xanthine oxidase (XOD) were determined biochemically. Total antioxidative capacity (T-AOC) and anti-superoxide anion capacity (A-SAC) were also determined. Ultrastructure of fibroblasts was observed under transmission electron microscope. The results showed that: UVB (1.176×10-4 J/cm2) suppressed the growth of fibroblasts and the introduction of PCF (0.25%-l%) before UVB reduced the suppression in a concentration-dependent manner. PCF could enhance the activities of SOD, GSH-PX and T-AOC as well as A-SAC. Also PCF could inhibit XOD activity, while it did not affect CAT activity. Ultrastructure of fibroblasts were damaged after UVB irradiation, concentration-dependent PCF reduced the destructive effect of UVB on cells. These results indicated that PCF can protect human dermal fibroblasts from being harmed by UVB irradiation via its antioxidant pro-erty.

Regulation of Eaf2 in mouse lens cells apoptosis induced by ultraviolet radiation

AIM: To investigate the regulation of Eaf2 protein in mouse lens cells apoptosis induced by ultraviolet (UV) radiation. METHODS: An eye of Eaf2 gene knockout mice or normal control mice was exposed to UV radiation, and the other one was non-exposed. All of lenses were analyzed by TUNEL and caspase 3 activity assays to determine the difference of the apoptosis induced by UV radiation. In addition, exposed and non-exposed lenses were analyzed by quantified p53 expression and real-time reverse transcription-polymerase chain reaction (RT-PCR) of Bax, Bid, Apaf-1, Puma and Noxa, to compare Eaf2 gene knockout mice and normal control mice. RESULTS: UV radiation caused apoptosis of lens cells in normal control mice and Eaf2 knockout mice. Activity of caspase 3 was significantly higher in normal control mice than Eaf2 knockout mice. Expression of p53 protein was significantly higher in lenses exposed to UV radiation than nonexposed lenses, but was similar between Eaf2 gene knockout mice and normal control mice in the same UV condition. After exposing to UV radiation, the analysis of real-time RT-PCR demonstrated that mRNA levels of Puma and Noxa were significantly higher in lenses of normal control mice than Eaf2 gene knockout mice, and that mRNA levels of Bax, Bid and Apaf-1 were not significantly different between gene knockout mice and normal control mice. CONCLUSION: Eaf2 increases lens cells apoptosis induced by ultraviolet radiation. And Eaf2 up-regulates expression of the Puma and the Noxa to act on lens cells apoptosis after UV radiation.

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.

Relationship between the morbidity of pterygium and the duration of ultraviolet rays exposure in Sanya,China

Pterygium is sunlight related, ocular-surface lesion that obscures vision. The morbidity varies in different parts of the same country. Several surveys have shown that the countries nearer the equator have higher rate of pterygium than the other regions, the possible reason is due to the low latitude and stronger exposure to ultraviolet rays. The onset of pterygium is closely related to the environment, including ultraviolet rays, sandstorm, dry climate and so on. Prolonged ultraviolet-B radiation is regarded as a risk factor for pterygium, and that could explain its prevalence is much higher in the low latitude area.

Changes of HSPs family expression in psoriasis lesions and their correlation with inflammatory response before and after NB-UVB treatment

Objective:To study the changes of HSPs family expression in psoriasis lesions and their correlation with inflammatory response before and after narrow-band ultraviolet B (NB-UVB) treatment.Methods: Patients who were newly diagnosed with psoriasis vulgaris and treated in Dermatology Department of our hospital between March 2015 and May 2017 were selected and randomly divided into the NB-UVB group who received NB-UVB combined with conventional treatment and the control group who received conventional treatment. Before treatment and 20 d after treatment, proper amount of psoriasis lesion was collected to determine the expression of HSPs family molecules and lymphocyte transcription factors as well as the levels of inflammatory cytokines.Results: Compared with those before treatment, HSP27, HSP60, HSP90 , HSP90β, T-bet and Foxp3 mRNA expression as well as MCP-1, IFN-γ and IL-17 levels in psoriasis lesion of both groups significantly decreased whereas GATA-3 and RORγt mRNA expression as well as IL-10 and TGF-β1 levels significantly increased after treatment, and HSP27, HSP60, HSP90 , HSP90β, T-bet and Foxp3 mRNA expression as well as MCP-1, IFN-γ and IL-17 levels in psoriasis lesion of NB-UVB group were significantly lower than those of control group whereas GATA-3 and RORγt mRNA expression as well as IL-10 and TGF-β1 levels were significantly higher than those of control group;HSP27, HSP60, HSP90 and HSP90β mRNA expression in psoriasis lesion of NB-UVB group after treatment were positively correlated with MCP-1, IFN-γ and IL-17 levels as well as T-bet and Foxp3 mRNA expression, and negatively correlated with IL-10 and TGF-β1 levels as well as GATA-3 and RORγt mRNA expression.Conclusion: NB-UVB treatment of psoriasis can reduce the expression of HSPs family members and inhibit the inflammatory response mediated by HSPs.

The effect of sunblock against oxidative stress in farmers：a pilot study

Farmers are frequently exposed to ultraviolet（UV） radiation which causes various diseases by inducing oxidative stress.This study aimed to assess the effects of sunblock on oxidative stress in the body.Eighty-seven farmers were divided into two groups：those who wore sunblock for five days and those who did not.The total antioxidant capacity（TAC） in urine,which is an antioxidant indicator,and 8-hydroxy-2-deoxyguanosine（8-OHdG） levels in urine,an oxidative stress indicator,were measured.The urinary TAC of sunblock users was significantly higher than that of non-users,but urinary 8-OHdG levels were not significantly different.Even after adjustment for potential confounders,urinary TAC was found to be markedly increased with sunblock usage.These results suggest that sunblock is effective in preventing oxidative stress among farmers.In addition,they show that urinary TAC can be used as a good effect marker of oxidative stress caused by UV exposure.

Green tea polyphenol epigallocatechin-3-gallate inhibits the expression of nitric oxide synthase and generation of nitric oxide induced by ultraviolet B in HaCaT cells

Background Nitic oxide （NO） has been implicated in the pathogenesis of various inflammatory diseases, including sunburn and pigmentation induced by ultraviolet irradiation. Epigallocatechin-3-gallate （EGCG） is the major effective component in green tea and can protect skin from ultraviolet-induced damage. The purpose of this study was to investigate the protective mechanisms of EGCG on inducible nitric oxide synthase （iNOS） expression and NO generation by ultraviolet B （UVB） irradiation in HaCaT cells. Methods HaCaT cells were irradiated with UVB 30 mJ/cm^2 and pretreated with EGCG at varying concentrations. The iNOS mRNA was detected by reverse transcriptase polymerase chain reaction （RT-PCR） and NO production was quantified by spectrophotometric method. The expression of NF-κB P65 was measured by immunofluorescence cytochemistry staining. Results The expression of iNOS mRNA and generation of NO in HaCaT cells were increased by UVB irradiation. EGCG down regulated the UVB-induced iNOS mRNA synthesis and NO generation in a dose dependent manner. The UVB-induced activation and translocation of NF-κB were also down regulated by EGCG treatment in HaCaT cells （P〈0.01）. Conclusions Green tea derived-EGCG can inhibit and down regulate the UVB-induced activation and translocation of NF-κB, expression of iNOS mRNA and generation of NO respectively, indicating EGCG may play a protective role from UVB-induced skin damage.

Curcumin from Jianghuang (Rhizoma Curcumae Longae) protects against exposure to ultraviolet B by antioxidation and attenuating mitochondrion-dependent apoptosis

OBJECTIVE:To investigate the protective effect of curcumin extracted from Jianghuang(Rhizoma Curcumae Longae)against ultraviolet B(UVB)and the possible mechanism.METHODS:Effects of curcumin were detected in vivo and in vitro.Morphological changes of white guinea pig skin were assessed by hematoxylin and eosin staining.Ha CaT cell proliferation was measured by 3-[4,5-dimethylthylthiazol-2-yl]-2,5 diphenyltetrazolium broide(MTT)assays.The cell cycle distribution,apoptotic rate,level of reactive oxygen species(ROS),mitochondrial membrane potential,and intracellullar calcium ion concentration of Ha CaT cells were detected by flow cytometry.Antioxidant levels in skin tissues and Ha Cat cells were measured by biochemical methods.RESULTS:UVB inhibited in vitro cell proliferation by inducing G2/M arrest,increasing ROS,apoptosis,and necrosis,and decreasing B-cell lymphoma-2,and increasing Bax,cytochrome c,and caspase-3 levels.CONCLUSION:Curcumin blocks the effects of UVB by reducing ROS and apoptosis,and reversing UVB-induced changes in the expression of apoptotic proteins.The mitochondrial pathway is involved in curcumin-regulated apoptosis.

IL-1α and ATP mRNA expression after ultraviolet lrradiation in human keratinocyte original-SCC 12F cells

Background Generally speaking, undifferentiated keratinocytes may synthesize a larger amount of IL-α and its production is decreased as cells complete differentiation gradually. Ultraviolet B (UVB) light can signigicantly stimulate the production and release of some cytokines. In this study we investigated the influence of UVB irradiation on IL-1α and adenosine triphosphoric (ATP) mRNA expressions in the human keratinocyte (KC) of original squamous cell carcinoma line (SCC 12F cells).Methods The cultured SCC 12F cells were irradiated with 30 mJ/cm 2 of UVB. Northern blot was employed to analyze the expression of IL-1α and ATP mRNA. Results There was a constitutive expression of IL-1α mRNA in SCC 12F cells. The expression increased in culturing time in regular KC medium and reached the highest expression at 120 hours. The expression level of IL-1α was up-regulated with two peaks at 6 hours and 72 hours, respectively after UVB irradiation. In comparison with IL-1α mRNA expression, ATP mRNA was down-regulated, with similar biphasic peaks, compared with the sham irradiated group. Conclusions SCC12F cells may express IL-1α mRNA constitutively. After UVB irradiation, the mRNA expression of IL-1α and ATP will show opposite effect because of inflammation/immunity and energy consumption mechanisms.

Nonlinear optical properties of a self-organized dye thin film

A self-organized thin film of a cyanine dye is fabricated by the spin-coating technique and is characterized by ultraviolet-visible spectroscopy, infrared （IR） spectroscopy, small-angle X-ray diffraction, eUipsometer, and atomic force microscopy （AFM）. The nonlinear optical properties of the thin films are investigated by degenerate four wave mixing （DFWM） technique. The cyanine dye thin film sample exhibits high optical nonlinearities （χ^（3） = 2.55 × 10^-12 esu）, and the mechanism is analyzed by the exciton coupling theory.

APP17肽通过抑制细胞内ROS保护紫外线照射后人皮肤成纤维细胞(英文)

Objective Ultraviolet light (UV) is known to cause photoaging of skin.UV irradiation can damage proliferation capacity and induce collagenase in fibroblasts in the dermis.Many researchers have explored the potential photo-protective agents;however,no ideal agent has been widely accepted.Amyloid precursor protein 17-mer peptide (APP17-mer peptide),an active peptide segment,has been reported to be responsible for the trophic effect in clonal CNS neuronal line,fibroblast cell line and HaCat cells.The aim of this study was to explore the effects of APP17-mer peptide on cultured fibroblasts after ultraviolet irradiation.Methods Human skin fibroblasts were cultured in DMEM medium with or without APP17-mer peptide (concentrations ranging from 20μmol/L,40 μmol/L,to 80μmol/L).The cultured fibroblasts were exposed to a single UV irradiation,and the proliferation activity of fibroblasts was detected by a MTT assay.The expression of matrix metalloproteinase-1 (MMP-1) mRNA was analyzed quantitatively following real-time RT-PCR.The generation of intracellular reactive oxygen species (ROS) was measured with fluorescent quantitation method.Results A single exposure to UV irradiation depressed proliferation activity of fibroblasts compared with sham-irradiated control (P<0.05).40μmol/L and 80μmol/L APP17-mer peptide increased the cellular proliferation activity in UV irradiated and unirradiated fibroblasts (P<0.05),however,20μmol/L did not show such protective effects (P>0.05).A single exposure of fibroblasts to UV irradiation resulted in 1.78 fold up-regulation of MMP-1 mRNA compared with unirradiated sample (P<0.05),and 40μmol/L and 80μmol/L APP17-mer peptide decreased the expression of MMP-1 mRNA (P<0.05 and P<0.01,respectively).UV irradiation increased generation of ROS in cultured fibroblasts (P<0.05).40μmol/L APP17-mer peptide inhibited the generation of ROS in irradiated fibroblasts.Conclusions APP17-mer peptide can enhance proliferation activity of fibroblasts after exposure to UV irradiation;it can also inhibit MMP-1 mRNA expression and ROS generation induced by UV irradiation.Inhibition of ROS generation after UV irradiation might be involved in the protective mechanism of APP17 peptide on proliferation activity and collagenase induction in UV-irradiated fibroblasts.