Number Of Sunburn Cells Research Articles

The Addition of Astaxanthin 0.5% in Sunscreen SPF 50 Inhibits the Increase of Sunburn Cells in Rats Induced By Ultraviolet Light B

Long-term exposure to ultraviolet light can cause chronic inflammation that can damage collagen and increase sunburn cells known as photoaging. There is a prevalence of up to 69% in female students in Jakarta aged 18–21 years who experience aging of the skin due to not using sunscreen. One of the signs of photoaging measured in this study is sunburn cells. This study wants to prove that the addition of astaxanthin 0.5% contained in SPF 50 sunscreen can inhibit the increase in sunburn cells in mice induced by ultraviolet B-light. Sunscreen also has protection limits, for example, SPF 30 has 97% protection, which means there is still 3% of radiation entering the skin so there is still a small portion that can cause free radicals. Additional ingredients are needed so that sunscreen can optimally protect the skin. An experimental study with a post-test-only design was used in this study comparing rats given SPF 50 sunscreen containing no astaxanthin (P1) and rats given SPF 50 sunscreen containing 0.5% astaxanthin (P2) to assess the inhibition of increased sunburn cells. 36 rats (Rattus Norvegicus) were divided into 2 groups and then shaved and exposed to UVB light with a total of 3100 mJ for 5 weeks. After the last exposure in the fifth week, skin tissue was taken fixed and stained using Hematoxylin Eosin to count sunburn cells. Sunburn Cells in group P1 had a value of 0.47 Å} 0.27 cells per high power field (hpf), and group P2 had a value of 0.16 Å} 0.18 cells per hpf. According to the Mann-Whitney test, there is a significant difference in the number of sunburn cells between groups (p < 0.05). From the results of this study, it can be concluded that astaxanthin 0.5% added to SPF 50 sunscreen products can inhibit the increase in sunburn cells.

Administration of Arabika Coffee Leaf Extract (Coffea Arabica) Reduces Tumor Necrosis Factor Alpha (TNF-α) and Sunburn Cell Levels in Male Wistar Rats (Rattus norvegicus) Exposed to Ultraviolet-B Rays

Background: Ultraviolet (UV) radiation has acute and chronic impacts on the skin. However, UVB exposure can be prevented with available natural ingredients, especially those containing antioxidants. One of the natural ingredients that contains active compounds as antioxidants is arabica coffee leaves, which contain flavonoids that have antioxidant effects. Methods: This study was an experimental research with a post-test-only control group design, using 30 male Wistar rats (Rattus norvegicus) which were divided into 5 groups; the control group (P0), treatment group 1 (P1) were given placebo, while group 2 (P2), group 3 (P3) and group 4 (P4) was given UVB rays and given ethanol extract cream from Arabica coffee leaves at a dose of 2,5%, 5%, and 10% respectively. Results: The average TNF- α levels in group P0, P1, P2, P3, and P4 were 97,88±1,19 ng/mL, 162,41±1,87 ng/mL, 138,04±1,03 g/mL, 124,71±2,65 ng/mL and 107,18±1,52 ng/mL. The average sunburn cells in P0, P1, P2, P3, and P4 were 4,0±0,13, 4,07±0,27, 2,60±0,25, 1,67±0,15 and 1,33±0,12 per field view. The administration of 10% Arabica coffee leaf extract cream was the most effective in reducing TNF-α levels by 34.01% (p<0.001) and has the lowest sunburn cells per field view (1,33±0,12 cell/field view; p < 0,001). Conclusion: Administration of ethanol extract cream from Arabica coffee leaves (Coffea arabica) can reduce TNF-α levels and the number of sunburn cells in the skin of male Wistar rats (Rattus norvegicus) exposed to UVB radiation.

Comparative Study of Liposomal and Ethosomal Formulations of Curcuma heyneana Rhizome Extract in a Transdermal Delivery System.

This study aimed to develop an anti-aging nanoformulation with Curcuma heyneana extract as bioactive substance. Curcuma heyneana Valeton & Zipj extract has been proven in previous research to have antioxidant, anti-ageing, anti-inflammatory, and wound healing properties, which makes it a potential bioactive material for anti-ageing and sunscreen cosmetic products. Phytoantioxidants need to penetrate into deeper skin layers to ensure effectivity. Thus, a transdermal delivery system is needed to deliver the extract to a deeper skin layer. The objective of the study was to compare the permeability and anti-ageing activity of liposomal and ethosomal formulations of C. heynena rhizome ethanolic extract. In this study, C. heyneana extract was loaded into a phospholipid vesicular system in the form of liposome and ethosome formulations using the ethanolic injection method. The anti-ageing activity was assessed by analyzing the epidermal thickness, number of sunburn cells, distance between collagen fibres, and number of fibroblasts. While the histologic specimen scoring was carried out for the in vivo penetration study. The ethosomal formulation had been found to have better penetration ability since it was able to reach the lower dermis area compared to the liposomes, which only reached the upper dermis. The ethosomal formulation of C. heyneana extract exhibited a better anti-ageing activity based on the parameters of epidermal thickness, sunburn cell count, fibroblast count, and the distance between collagen fibres in rat skin histology. Ethosomes have been found to be a more proficient carrier system for transdermal delivery of C. heyneana extract compared to liposomes. Meanwhile, their penetration correlated with the effectivity of the formulation, suggesting that the vesicular system enhanced the penetration ability of the extract.

The Effectiveness of Snail (Achatina Fulica) Slime Cream toward Inhibiting the Formation of Sunburn Cells on Mice (Mus Musculus) Balb/C Skin (Experimental Study with Induced UVB Radiation)

Background ─ Sunburn is a radiation burn of the skin by exposure to UV light. UVB is the most dangerous UV light for humans and can cause skin cancer risk. UVB rays can damage DNA so that it can cause a response in the form of apoptosis of keratinocyte cells or also called sunburn cells. Objective ─ Determined the effectiveness of snail (Achatina fulica) slime cream on inhibited the formation of sunburn cells on the skin of BALB/c mice (Mus musculus) induced by UVB radiation. Metodhs ─ Experimental research using randomized post-test only control group design with 35 male BALB/c (Mus musculus) mice divided into 7 groups. There was a group without treatment, a negative control group, a control group with Parasol Face Sunscreen Cream, and 4 treatment groups with topical application of snail slime cream with varying doses. All groups except the untreated group were irradiated with UVB 200 mJ/cm2 for 1x irradiation. The mice’s back skin was taken 24 hours later to make histology slide and sunburn cell counting. Data were analyzed using One Way ANOVA comparative test, Post-hoc LSD test, and Spearman's rho correlative test with each significance value p<0.05. Results ─ There are a significant difference in the mean number of sunburn cells in One Way ANOVA test p=0.00 (p<0.05) between all groups. LSD post-hoc test shows the group with the most significant mean difference (16.20) was between the negative control group and treatment group 4 (X4) with p=0.00 (p<0.05). There is a relationship between the dose of snail slime cream and the percentage of sunburn cells in the Spearman's rho test with p=0.00 (p<0.05) and the strength of the relationship between the dose of snail slime cream and the percentage of sunburn cells is very strong indicated by the Pearson Correlation (r)= -0.900. Conclusion ─ Snail slime cream effectively inhibits the formation of sunburn cells with the most effective dose in this study is the 10% dose.

The extract of Red Beetroot (Beta vulgaris L.) Prevent Tumor Necrosis Factor-Alpha (TNF-?) Levels and Prevent Increased Sunburn in Epidermal Cell in Rats Exposed to UVB

Backgrounds: UVB radiation can also cause acute changes, such as sunburn and pigmentation, and chronic changes, such as photocarcinogenesis and immunosuppression. The betalain compound in beetroot extract also functions as a potent anti-inflammatory agent. Method: This study employed a true experimental study with a randomized post-test only control group design using 30 rats divided into three groups for treat 28 days. The negative control used placebo and without exposure to UVB (K1). The positive control group exposed to UVB and get placebo (K2). The treatment group get exposed to UVB light and treated red beetroot extract at a dose of 500 mg/kg BW via oral (K3). TNF-? levels were measured using ELISA. Sunburn cells were measured by observing the epidermal cells under a microscope. Statistical using one-way ANOVA with significantly p<0.05. Results: TNF-? levels in K1 was 33.464?1.533 ng/L, K2 was 47.546?4.194 ng/L, and K3 was 32.625?0.839 ng/L. The number of sunburn cells in K1 was 0.280?0.611 cells/visual field K2 was 0.980?0.121 cells/HPF, and K3 was 0.300?0.054 cells/HPF. Based on the results of the Post-hoc (LSD) analysis, TNF-? levels in K3 decreased significantly compared to K2 (p=0.000), while TNF-? levels in K3 were not significantly different from K1 (p=0.824). Similarly, the number of sunburn cells in K3 decreased significantly compared to K2 (p=0.000), while the number of sunburn cells in K3 did not differ significantly from K1 (p=0.665). Conclusion: red beetroot extract can prevent inflammatory factor TNF-? and increased sunburn of epidermal cells in rats exposed to UVB.

Development of skin health test efficacy modules in vivo

Sunlight contains ultraviolet (UV) light that causes sunburn and makes the skin age faster, leading to more wrinkles as older. The UV light can come from the natural and artificial sources. Moreover, UV light has shorter wavelengths than the visible light. Therefore, people’ eyes can’t see UV, but people’ skin can feel it. In this study, the in vivo skin health test efficacy modules have been established via the detection of skin’s moisture retention (%), skin’s cytokine expression levels, enzymatic expressions in the skin, the expression levels of hyaluronic acid (HA), collagen type I, melanin, and malondialdehyde (MDA) in the skin, and the experimental mice’ skin thickness and lesions via histo-pathologic examination. According to the results, the clinical behavior observation indexes of Institute of Cancer Research (ICR) mice in each group were normal during the experiments. Moreover, all ICR mice were survival until the end of the experiments. The moisture retention (%) of skin in ICR mice in UVB group was significant decrease after D1, D3, and D5 of UVB irradiation compared to the normal control group. Based on the IL-1β, IL-6 and TNF-α analysis expressions, both IL-1β and IL-6 expressions in UVB group were significantly increase than the control group, while there was no significant difference in the TNF-α expression between the groups. ICR mice’ skin enzymatic expressions in each group presented that catalase (CAT) expression and superoxide dismutase (SOD) activity in UVB group were significantly lower than the control group. The MDA expression in UVB group were significantly higher than the control group. The HA and collagen type I expressions in UVB group were significantly lower than the control group. However, the melanin expressions in UVB group and the control groups were not significantly different. The matrix metalloproteinase 2 (MMP-2) expressions in UVB group was significantly higher than the control group. The skin epidermal thickness in UVB group was significantly thicker than the control group. The dermal thickness in two groups was not significantly different. The number of sunburn cells in the derma in UVB group was significantly increase than the control group. The solar elastosis in the derma in two groups was not significantly different. Based on the above results, we have successfully established in vivo skin health test efficacy modules to evaluate the status of skin health. We hope the modules should be provide for the research and development (R&amp;D) of the effective treatment included drugs and therapeutic strategies.

291 In vitro efficacy of a sunscreen (50+) and octatrienoic acid 0.1% in actinic keratosis and UVs damages

Actinic keratosis (AK) is a form of dysplastic epidermal lesions resulting from chronic and excessive UV exposure with a certain risk to become cancerous. The use of sunscreens to prevent photodamages is advocated by the current guidelines on AK treatment. To be efficient a photoprotection has to involve UV filters but also secondary factors such as antioxidants and anti-inflammatory agents able to counteract the photochemical and genetic cascade triggered by UVs. In the present work we used an in vitro model of human skin (Phenion® Ft) in order to assess the photoprotective potential of a sunscreen containing inorganic sun-filters (50+ SPF) and 0.1% octatrienoic acid (KERA’+) after UVA (10J/cm2) and UVB (25mJ/cm2) by mean of evaluation of the number of sunburn cells and apoptotic keratinocytes.

Protective effects of sunscreen (50+) and octatrienoic acid 0.1% in actinic keratosis and UV damages

Actinic keratosis is a form of dysplastic epidermal lesion resulting from chronic and excessive UV exposure with a certain risk of becoming cancerous. Current guidelines advocated the use of sunscreens...

Photochemoprotective Potential of the Ethyl Acetate Fraction from Eugenia hiemalis Leaves and Its 2,6-Di-O-galloylarbutin Isolate Against UVB-Induced Photodamage.

Intense and constant exposure to UVB radiation can lead to inflammation and oxidative stress, which are associated with many cutaneous disorders, including photoaging and skin cancer. Antioxidant plant materials that are rich in polyphenols, such as the ethyl acetate fraction (EAF) from Eugenia hiemalis leaves, and phenolic compounds represent a promising approach to protect the skin against UVB-induced damage. The present study evaluated the photochemoprotective potential of the EAF and its 2,6-di-O-galloylarbutin (1) isolate. The EAF and the phenolic antioxidant (1) reduced UVB-induced L929 fibroblast death. The EAF prevented UVB-induced damage in fibroblasts by inhibiting the intracellular production of reactive oxygen species and lipid peroxidation, especially in pretreated cells. Topical treatment with an emulsion with 1% EAF prevented/attenuated UVB-induced inflammation and oxidative stress in the skin in hairless mice by controlling the increase in myeloperoxidase activity, reducing superoxide anion production, maintaining radical-scavenging ability and ferric reducing power, and controlling the depletion of reduced glutathione and catalase levels. The EAF also inhibited the increase in epidermal thickness, mast cell infiltration, the number of sunburn cells and collagen fiber destruction that were triggered by UVB. The invitro and invivo results indicated that the EAF is a bioactive agent that is able to protect the skin against the harmful effects of UVB.

The Administration of Topical Aloe vera Extract Reduce the Number of Sunburn Cells and Expression of Caspase-3 on Post UVB-light-exposure Epidermis

Introduction : Ultraviolet B (UVB) radiation triggers the formation of free radicals that cause apoptosis and sunburn cells (SBC) formation. Aloe vera contains anti-inflammatory and antioxidant compounds that can potentially inhibit this process. Objective : to assess the effect of topical Aloe vera extract administration on the decrease of SBC number and Caspase-3 expression on the epidermis after UVB light exposure. Methods : In a post-test only group design study, a single dose of 3 doses of Erythema (DEM) was performed on two groups of 6 week old BALB/c female rats. Group A (control) did not receive any topical treatment, and group B (treatment) were smeared with 75% Aloe vera extract before irradiation. Each group was divided into 4 sub-groups based on post-exposure time of 6 hours (A1 and B1), 12 hours (A2 and B2), 24 hours (A3 and B3), and 48 hours (A4 and B4). The expression of caspase-3 was assessed by immunohistochemical staining while the SBC number was measured using a microscope. The expression of caspase-3 was analyzed using the Kruskal-Wallis and Mann-Whitney statistical tests, while the number of SBC was analyzed using the one-way ANOVA statistical test and the post-hoc LSD test. Results : The results of the Kruskal-Wallis analysis showed a significant difference in Caspase-3 expression between groups, p <0.05. The results of Mann-Whitney analysis showed a significant difference in Caspase-3 expression between the A1-A3 and B1-B3 subgroups (p <0.05). One-way ANOVA analysis showed a significant difference in the number of SBC between groups (p <0.05). Post-hoc LSD analysis showed significant differences in SBC counts between groups A and B across all subgroups, p <0.05. Conclusion : Topical application of Aloe Vera extract decreased Caspase-3 expression and the number of SBC in UVB light-exposed skin.

Java plum (Syzygium cumini) extract cream effect on decreasing the number of sunburn cell on the dorsal skin of male Wistar rat (Rattus norvegicus) exposed to UV-radiation

Background: The primary acute damage due to UV radiation is keratinocyte apoptosis or sunburn cell. Previous studies showed that antioxidants inhibit UV damage. Java plum (Syzygium cumini) which is found in Indonesia, was known to have a high concentration of antioxidants. This study was aimed to assess the Java plum ethanol extract cream effects on the number of sunburn cells on the dorsal skin of male Wistar rats that exposed to UV-B.&#x0D; Methods This experimental research was a post-test only control group design that was conducted on 30 male rats. Groups were divided into control, placebo, 5%, 10%, and 20% ethanol extract cream concentrations (P1, P2, P3, P4, and P5, respectively). The number of sunburn cell were then observed and recorded based on visual evaluation of the skin biopsy under a light microscope.&#x0D; Results: The mean results of P1, P2, P3, P4, and P5 were 132.67, 98.67, 118.67, 104.00, and 54.67 respectively. The control, placebo, 5%, and 10% ethanol extract cream showed no significant result (p&gt;0.05). In contrast, 20% ethanol extract cream showed a protective effect (p&lt;0.05).&#x0D; Conclusion: Java plum ethanol extract cream with 20% dose could decrease the number of sunburn cells in the skin.

5-aminolaevulinic acid-based photodynamic therapy inhibits ultraviolet B-induced skin photodamage.

To evaluate the photoprotective effect of 5-aminolaevulinic acid-based photodynamic therapy (ALA-PDT) on ultraviolet B (UVB)-induced skin photodamage. In vivo experiments, the dorsal skin of hairless mice were treated with ALA-PDT or saline-PDT, and then exposed to 180 mJ/m2 UVB. Results showed that the number of sunburn cells and apoptotic cells in the epidermis of ALA-PDT-treated groups at 24 h after UVB irradiation were significantly decreased compared with those in the UVB groups. And the removal rate of CPDs was obviously higher in ALA-PDT-treated groups. At 48 h, the number of Ki67 positive nuclei in ALA-PDT-UVB group was significantly fewer than that in UVB group. Further in vitro experiments, human keratinocyte cell line (HaCaT) cells of two groups (one treated with ALA-PDT, the other untreated), were exposed to 60 mJ/m2 UVB irradiation. We found 0.5 mmol/L of ALA and 3 J/cm2 of red light did not affect the vitality of cells, and could reduce UVB induced apoptosis, accelerate the clearance of CPDs, inhibit proliferation and activate p53. Thus, our data demonstrate that ALA-PDT pretreatment can induce a protective DNA damage response that protects skin cells from UVB-induced photodamages.

Retraction: (-)-Epigallocatechin-3-Gallate Prevents Photocarcinogenesis in Mice through Interleukin-12-Dependent DNA Repair.

We have shown previously that topical application of (-)-epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, prevents photocarcinogenesis in mice. EGCG prevents UVB-induced immunosuppression by inducing interleukin-12 (IL-12). As immunosuppression is a risk factor for photocarcinogenesis, we investigated the possibility that EGCG also prevents UVB-induced photocarcinogenesis through an IL-12-dependent DNA repair mechanism. To investigate this possibility, we determined the effects of EGCG on photocarcinogenesis in IL-12 knockout (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of the extent of UVB-induced DNA damage. Topical application of EGCG (1 mg/cm(2) skin) prevented photocarcinogenesis in wild-type (C3H/HeN) mice in terms of tumor incidence and tumor multiplicity but did not prevent photocarcinogenesis in IL-12 KO mice. UVB-induced DNA damage, as determined by the formation of CPDs and the number of sunburn cells, was resolved more rapidly in the skin of wild-type mice treated with EGCG than untreated control mice. In contrast, the extent of UVB-induced DNA damage and the numbers of sunburn cells were not significantly different in the EGCG-treated IL-12 KO mice and untreated control mice. In addition, treatment of XPA-proficient human fibroblast cells with EGCG promoted repair of UVB-induced CPDs in a dose-dependent manner but not in an XPA-deficient cells, indicating that the nucleotide excision repair mechanism is involved in EGCG-mediated DNA repair. Taken together, these results indicate for the first time that EGCG can prevent photocarcinogenesis through an EGCG-induced IL-12-dependent DNA repair mechanism.

Serotonin signalling is crucial in the induction of PUVA-induced systemic suppression of delayed-type hypersensitivity but not local apoptosis or inflammation of the skin.

Psoralen and UVA (PUVA) has immunosuppressive and proapoptotic effects, which are thought to be responsible alone or in combination for its therapeutic efficacy. However, the molecular mechanism by which PUVA mediates its effects is not well understood. Activation of the serotonin (5-hydroxytryptamine, 5-HT) pathway has been suggested to be involved in the modulation of T-cell responses and found to mediate UVB-induced immune suppression. In particular, the activation of the 5-HT2A receptor has been proposed as one mechanism responsible for UV-induced immune suppression. We therefore hypothesized that 5-HT may play a role in PUVA-induced effects. The model of systemic suppression of delayed-type hypersensitivity (DTH) to Candida albicans was used to study immune function after exposure of C3H and KIT(W) (-Sh/W-Sh) mice to a minimal inflammatory dose of topical PUVA. The intra-peritoneal injection of the 5-HT2 receptor antagonist ketanserin or cyproheptadine or an anti-5-HT antibody immediately before PUVA exposure entirely abrogated suppression of DTH but had no significant effect on inflammation, as measured by swelling and cellular infiltration of the skin, and apoptosis as determined by the number of sunburn cells in C3H mice. Importantly, the systemic injection of 5-HT recapitulated PUVA immune suppression of DTH but did not induce inflammation or apoptosis in the skin. KIT(W) (-Sh/W-Sh) mice (exhibiting myelopoietic abnormalities, including lack of 5-HT-containing mast cells) were resistant to PUVA-induced suppression of DTH but not local skin swelling. Thus, this points towards a crucial role of 5-HT signalling in PUVA-induced immune suppression but not inflammation or apoptosis insitu in the skin.

Protective Effect of Chitin Urocanate Nanofibers against Ultraviolet Radiation.

Urocanic acid is a major ultraviolet (UV)-absorbing chromophore. Chitins are highly crystalline structures that are found predominantly in crustacean shells. Alpha-chitin consists of microfibers that contain nanofibrils embedded in a protein matrix. Acid hydrolysis is a common method used to prepare chitin nanofibrils (NFs). We typically obtain NFs by hydrolyzing chitin with acetic acid. However, in the present study, we used urocanic acid to prepare urocanic acid chitin NFs (UNFs) and examined its protective effect against UVB radiation. Hos: HR-1 mice coated with UNFs were UVB irradiated (302 nm, 150 mJ/cm2), and these mice showed markedly lower UVB radiation-induced cutaneous erythema than the control. Additionally, sunburn cells were rarely detected in the epidermis of UNFs-coated mice after UVB irradiation. Although the difference was not as significant as UNFs, the number of sunburn cells in mice treated with acetic acid chitin nanofibrils (ANFs) tended to be lower than in control mice. These results demonstrate that ANFs have a protective effect against UVB and suggest that the anti-inflammatory and antioxidant effects of NFs influence the protective effect of ANFs against UVB radiation. The combination of NFs with other substances that possess UV-protective effects, such as urocanic acid, may provide an enhanced protective effect against UVB radiation.

Sulforaphane and phenylethyl isothiocyanate protect human skin against UVR-induced oxidative stress and apoptosis: Role of Nrf2-dependent gene expression and antioxidant enzymes

Chronic UVR-exposure may impair the stress response and antioxidant defense mechanisms of human skin. The transcription factor nuclear factor erythroid-2 related factor 2 (Nrf2) orchestrates the expression of genes coding for the stress response and antioxidant proteins. Here, we tested sulforaphane (SFN) and phenylethyl isothiocyanate (PEITC) for their ability to counteract UVR-induced oxidative stress and apoptosis in ex vivo human full-thickness skin combined with in vitro HaCaT keratinocytes. Investigation of Nrf2 transactivation and induction of genes coding for Nrf2-dependent phase II antioxidative enzymes (γ-glutamylcysteine-synthetase (γGCS), heme oxygenase 1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1)) was performed in HaCaT keratinocytes. Comparative investigations in human ex vivo skin were conducted for analysis of gene expression of above mentioned phase II enzymes and catalase (CAT) as well as hematoxylin/eosin (H&E) and immunofluorescence (catalase, cleaved Casp-3). UVR exposure of human skin (300mJ/cm2) resulted in a significant time-dependent increase of the number of sunburn cells and caspase-3 activation as biomarkers of apoptosis for up to 48h (p<0.001) and induced a significant decrease of the antioxidant enzyme catalase (p<0.001). This was significantly counteracted by the pre-treatment of human skin with SFN and PEITC (5μM and 10μM). Mechanistic cell culture studies revealed SFN and PEITC to increase Nrf2 activity and Nrf2-dependent gene expression (γGCS, HO-1, NQO1); this was paralleled in human full skin mRNA. In conclusion, the induction of Nrf2-dependent antioxidant pathways seems to be a potential mechanism by which SFN and PEITC protect against UVR-induced oxidative stress and apoptosis in human skin.

Relationship between skin color and skin response to ultraviolet light

Relationship between skin color and skin response to ultraviolet light

Resveratrate protects human skin from damage due to repetitive ultraviolet irradiation

Ultraviolet (UV) exposure results in the production reactive oxygen species. Resveratrol has attracted considerable attentions owing to its natural abundance and multiple biological effects. To investigate the protective effects of resveratrate against damage to human skin induced by repetitive solar simulator ultraviolet radiation (ssUVR). Fifteen healthy volunteers were enrolled, and six sites on the non-exposed dorsal skin of each volunteer were marked for study. Sites 1-4 were exposed to ssUVR at a dosage of 1.5 minimal erythema dose for consecutive 4 days. Immediately after each exposure, one test material (resveratrate + antioxidant, antioxidant, resveratrate, vehicle) was applied to one of the four sites. Site 5 and site 6 were marked as positive control site (UVR only) and baseline control site (no treatment, no UVR). L*a*b values were assessed preprocedure and postprocedure. Skin biopsies were taken 24 h after the last irradiation. The specimens were stained to determine the number of sunburn cells and melanin content melanin. On resveratrate treated sites, erythema was barely seen with only slight decrease of L value and insignificant increase of *a value. Furthermore, resveratrate significantly inhibited sunburn cell formation, and decreased Fontana-Masson staining in skin samples. Resveratrate exerts protective effects against repetitive ssUVR-induced sunburn and suntan.

Topical Grape Seed Proanthocyandin Extract Reduces Sunburn Cells and Mutant p53 Positive Epidermal Cell Formation, and Prevents Depletion of Langerhans Cells in an Acute Sunburn Model

The purpose of this study was to investigate whether grape seed proanthocyanidin extract (GSPE) can provide photoprotection against ultraviolet (UV) irradiation. Study has shown that GSPE is a natural oxidant, and is used in many fields such as ischemia-reperfusion injury, chronic pancreatitis, and even cancer. However, the effect of GSPE on UV irradiation is as yet unknown. Cutaneous areas on the backs of normal volunteers were untreated or treated with GSPE solutions or vehicles 30 min before exposure to two minimal erythema doses (MED) of solar simulated radiation. Cutaneous areas at different sites were examined histologically for the number of sunburn cells, or immunohistochemically for Langerhans cells and mutant p53 epidermal cells. On histological and immunohistochemical examination, skin treated with GSPE before UV radiation showed fewer sunburn cells and mutant p53-positive epidermal cells and more Langerhans cells compared with skin treated with 2-MED UV radiation only (p<0.001, p<0.001, and p<0.01, respectively). GSPE may be a possible preventive agent for photoprotection.

Silymarin Protects Epidermal Keratinocytes from Ultraviolet Radiation-Induced Apoptosis and DNA Damage by Nucleotide Excision Repair Mechanism

Solar ultraviolet (UV) radiation is a well recognized epidemiologic risk factor for melanoma and non-melanoma skin cancers. This observation has been linked to the accumulation of UVB radiation-induced DNA lesions in cells, and that finally lead to the development of skin cancers. Earlier, we have shown that topical treatment of skin with silymarin, a plant flavanoid from milk thistle (Silybum marianum), inhibits photocarcinogenesis in mice; however it is less understood whether chemopreventive effect of silymarin is mediated through the repair of DNA lesions in skin cells and that protect the cells from apoptosis. Here, we show that treatment of normal human epidermal keratinocytes (NHEK) with silymarin blocks UVB-induced apoptosis of NHEK in vitro. Silymarin reduces the amount of UVB radiation-induced DNA damage as demonstrated by reduced amounts of cyclobutane pyrimidine dimers (CPDs) and as measured by comet assay, and that ultimately may lead to reduced apoptosis of NHEK. The reduction of UV radiation-induced DNA damage by silymarin appears to be related with induction of nucleotide excision repair (NER) genes, because UV radiation-induced apoptosis was not blocked by silymarin in NER-deficient human fibroblasts. Cytostaining and dot-blot analysis revealed that silymarin repaired UV-induced CPDs in NER-proficient fibroblasts from a healthy individual but did not repair UV-induced CPD-positive cells in NER-deficient fibroblasts from patients suffering from xeroderma pigmentosum complementation-A disease. Similarly, immunohistochemical analysis revealed that silymarin did not reduce the number of UVB-induced sunburn/apoptotic cells in the skin of NER-deficient mice, but reduced the number of sunburn cells in their wild-type counterparts. Together, these results suggest that silymarin exert the capacity to reduce UV radiation-induced DNA damage and, thus, prevent the harmful effects of UV radiation on the genomic stability of epidermal cells.