Model Of Photodamage Research Articles

Curcumin-Loaded Liposomes in Gel Protect the Skin of Mice against Oxidative Stress from Photodamage Induced by UV Irradiation.

Prolonged exposure to ultraviolet (UV) irradiation can cause oxidative stress in the skin, accompanied by rapid immunosuppressive effects, resulting in a peroxidation reaction throughout the body. Curcumin (Cur), as the bioactive compound of turmeric, is a natural polyphenol with potent antioxidant properties but is often overlooked due to its poor solubility and low bioavailability. In this study, curcumin-loaded liposomes in a sodium alginate gel complex preparation were designed to improve the bioavailability of curcumin and to study its preventive effect on photodamage. Cur-loaded liposomes (Cur-L), Cur-loaded gel (Cur-G) based on an alginate matrix, and curcumin-loaded liposomes in gel (Cur-LG) were prepared, and their antioxidant effects and drug diffusion abilities were evaluated. The antioxidant capacity of Cur, Cur-L, Cur-G, and Cur-LG was also studied in a mouse model of photodamage. Cur had the highest antioxidant activity at about 4 mg/mL. Cur-LG at this concentration showed antioxidant effects during 1,1-diphenyl-2-trinitrophenylhydrazine (DPPH) and H2O2 experiments. During the UV light damage test, Cur-LG demonstrated the ability to effectively neutralize free radicals generated as a result of lipid peroxidation in the skin, serum, and liver, thereby enhancing the overall activity of superoxide dismutase (SOD). In conclusion, using Cur-LG may protect against epidermal and cellular abnormalities induced by UV irradiation.

KGF-2 ameliorates UVB-triggered skin photodamage in mice by attenuating DNA damage and inflammatory response and mitochondrial dysfunction.

Long-term exposure to UVB induces DNA damage, inflammatory response, mitochondrial dysfunction, and apoptosis in skin cells, thus causing skin photodamage. Research has demonstrated the noteworthy antioxidant, anti-inflammatory, DNA repair, and mitochondrial protective properties of keratinocyte growth factor-2 (KGF-2). To examine the impact of KGF-2 on UVB-triggered skin photodamage in mice, hair-removed mice were initially exposed under UVB radiation and subsequently treated with KGF-2 hydrogel and repeated for 6 days. On day 7, the assessment of histopathological alterations, inflammation, DNA damage, mitochondrial function, and apoptosis in mouse skin was assessed. It was found that KGF-2 could effectively relieve cutaneous photodamage symptoms and inhibit epidermal proliferation in mice. Meanwhile, KGF-2 was found to significantly reduce DNA damage, attenuate the inflammatory response, and inhibit the mitochondria-mediated intrinsic apoptotic pathway in the UVB-exposed mouse skin photodamage model. To summarize, our results indicated that KGF-2 reduces the severity of mouse skin photodamage caused by UVB rays by attenuating DNA damage and the inflammatory response, besides inhibiting the mitochondria-mediated intrinsic apoptosis pathway.

High molecular weight hyaluronic acid-liposome delivery system for efficient transdermal treatment of acute and chronic skin photodamage

Photodamage is one of the most common causes of skin injury. High molecular weight hyaluronic acid (HHA) has shown immense potential in the treatment of skin photodamage by virtue of its anti-inflammatory, reparative, and antioxidative properties. However, due to its large molecular structure of HHA, HHA solution could only form a protective film on the skin surface in conventional application, failing to effectively penetrate the skin, which necessitates the development of new delivery strategies. Liposomes, with a structure similar to biological membranes, have garnered extensive attention as transdermal drug delivery carriers because of their advantages in permeability, dermal compatibility, and biosafety. Herein, we have developed a HHA-liposome transdermal system (HHL) by embedding HHA into the liposome structure using reverse evaporation, high-speed homogenization, and micro-jet techniques. The effective penetration and long-term residence of HHA in skin tissue were multidimensionally verified, and the kinetics of HHA in the skin were extensively studied. Moreover, it was demonstrated that HHL significantly strengthened the activity of human keratinocytes and effectively inhibits photo-induced cellular aging in vitro. Furthermore, a murine model of acute skin injury induced by laser ablation was established, where the transdermal system showed significant anti-inflammatory and immunosuppressive properties, promoting skin proliferation and scar repair, thereby demonstrating immense potential in accelerating skin wound healing. Meanwhile, HHL significantly ameliorated skin barrier dysfunction caused by simulated sunlight exposure, inhibited skin erythema, inflammatory responses, and oxidative stress, and promoted collagen expression in a chronic photodamage skin model. Therefore, this transdermal delivery system with biocompatibility represents a promising new strategy for the non-invasive application of HHA in skin photodamage, revealing the significant potential for clinical translation and broad application prospects. Statement of significanceThe transdermal system utilizing hyaluronic acid-based liposomes enhances skin permeability and retains high molecular weight hyaluronic acid (HHL). In vitro experiments with human keratinocytes demonstrate significant skin repair effects of HHL and its effective inhibition of cellular aging. In an acute photodamage model, HHL exhibits stronger anti-inflammatory and immunosuppressive properties, promoting skin proliferation and scar repair. In a chronic photodamage model, HHL significantly improves skin barrier dysfunction, reduces oxidative stress induced by simulated sunlight, and enhances collagen expression.

Bacillus amyloliquefaciens Lysate Ameliorates Photoaging of Human Skin Fibroblasts through NRF2/KEAP1 and TGF-β/SMAD Signaling Pathways

More and more research in dermatology and cosmetic science is devoted to the development and application of postbiotic raw materials. In order to explore the anti-photoaging efficacy and application prospect of Bacillus amyloliquefaciens lysate (BAL1) on the skin, we used 16 J/cm2 UVA stimulation of human embryonic fibroblasts (CCC-ESF-1) to establish a UVA photodamage model to investigate the anti-photoaging efficacy of BAL1 and its mechanism of action. In this study, we found that BAL1 activated the transcription of downstream antioxidant enzyme genes mainly by promoting the nuclear displacement of NF-E2-related factor 2 (Nrf2) within CCC-ESF-1, thus increasing the antioxidant capacity of antioxidant enzymes to scavenge excessive reactive oxygen species in cells. Meanwhile, BAL1 promoted intracellular TGF-β/Smad signaling pathway and reduced matrix metalloproteinase expression to alleviate the degradation of extracellular matrix. In conclusion, the results of this study demonstrate the potential benefit of BAL1 in protecting the skin against UVA-induced photoaging and highlight the potential of BAL1 in skin photoprotection.

Lycium barbarum polysaccharide promotes proliferation of human melanocytes via activating the Nrf2/p62 signaling pathway by inducing autophagy in vitro.

Vitiligo is a skin disease characterized by lack of functional melanocytes. Lycium barbarum polysaccharide (LBP) has been demonstrated to preserve keratinocytes and fibroblasts against oxidative stress. This study aimed to explore the efficacy and underlying mechanisms of LBP on autophagy in H2 O2 -damaged human melanocytes. Cellular viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and annexin V-fluorescein isothiocyanate/propidium iodide double staining. Reverse transcription-polymerase chain reaction, western blotting and electron microscopy were performed to detect autophagy. The protein expression level of Nrf2 and p62 were assessed by western blotting. Plasmid transfection and lentiviral infection were used to overexpress and silence Nrf2 in PIG1 cells. LBP promoted the proliferation and inhibited apoptosis of H2 O2 -damaged PIG1 cells. LBP increased the proliferation of H2 O2 -damaged PIG1 cells via induction of autophagy, and Nrf2 shRNA experiment confirmed that LBP activated the Nrf2/p62 signal pathway. These results suggest that LBP may be used for the treatment of vitiligo. PRACTICAL APPLICATIONS: Goji berry is the mature and dried fruit of Lycium barbarum L., which is a common food with a long history in China, as well as a Traditional Chinese Medicine. Our previous research found that LBP could activated the Nrf2/ARE pathway in an ultraviolet (UV)-induced photodamage model of keratinocytes, and increase the levels of phase II detoxification and antioxidant enzymes. We firstly confirmed the anti-vitiligo effects of L. barbarum polysaccharide (LBP) by inducing autophagy and promoted proliferation of human melanocytes, and LBP induced autophagy via activating the Nrf2/p62 signaling pathway in this study. These results proved that LBP can be an effective therapy for vitiligo treatment.

The phenolic acids from Oplopanax elatus Nakai stems and their potential photo-damage prevention activity.

25 phenolic acids, including four new isolates, eurylophenosides A-D (1-4) and 21 known ones (5-25) were isolated and identified from the stems of Oplopanax elatus Nakai. Among the known compounds 5-9, 11-13, 16, 18-25 were isolated from the genus for the first time; 17 was first obtained from the plant; and the NMR data of 22 was reported here first. Meanwhile, the UVB-induced photodamage model of HaCaT cells was used to study the prevent-photodamage abilities of compounds 1-2, 4-8, 11-13 and 15-25 with a nontoxic concentration at 50μM. Moreover, a dose-dependent experiment was conducted for active compounds at the concentration of 10, 25, and 50µM, respectively. Consequently, pretreatment with compounds 1, 16, 17, 19, 20, 22, 24 and 25 could suppress the cell viability decreasing induced by UVB irradiation in a concentration-dependent manner. These results indicated that phenolic acids were one kind of material basis with prevent-photodamage activity of O. elatus.

Panax ginseng C. A. Meyer Phenolic Acid Extract Alleviates Ultraviolet B-Irradiation-Induced Photoaging in a Hairless Mouse Skin Photodamage Model.

Here, we evaluated the in vivo skin-protective effects of topical applications of Panax ginseng C. A. Meyer extract (PG2) and its phenolic acid- (PA-) based components against UVB-induced skin photoaging. PG2 or PA applied to skin of hairless mice after UVB-irradiation alleviated UVB-induced effects observed in untreated skin, such as increased transepidermal water loss (TEWL), increased epidermal thickness, and decreased stratum corneum water content without affecting body weight. Moreover, PG2 and PA treatments countered reduced mRNA-level expression of genes encoding filaggrin (FLG), transglutaminase-1 (TGM1), and hyaluronan synthases (HAS1, HAS2, and HAS3) caused by UVB exposure and reduced UVB-induced collagen fiber degradation by inhibiting the expression of matrix metalloproteinase genes encoding MMP-1, MMP-2, and MMP-9. Meanwhile, topical treatments reduced cyclooxygenase-2 (COX-2) mRNA-level expression in photodamaged skin, leading to the inhibition of interleukin-1β (IL-1β) and interleukin-6 (IL-6) mRNA-level expression. Thus, ginseng phenolic acid-based preparations have potential value as topical treatments to protect skin against UVB-induced photoaging.

Platelet-rich plasma regulating the repair of ultraviolet B–induced acute tissue inflammation: adjusting macrophage polarization through the activin receptor–follistatin system

ABSTRACT Ultraviolet B (UVB) is one of the most common exogenous factors in skin aging, especially photoaging. Once a large amount of UVB accumulates within a short period of time, skin tissue can become inflamed. It has also been found in clinics that platelet-rich plasma (PRP) can promote wound repair; therefore, the aim of this study was to identify the mechanism by which PRP repairs UVB-induced skin photodamage. We used PRP of Sprague-Dawley rats with the two-spin technique in the established acute UVB radiation photodamage model and harvested the corresponding skin after 1, 7, and 28 d. Hematoxylin and eosin staining was used to observe tissue inflammation. We found that PRP reduces inflammation in the early stages of UVB-induced acute skin damage, and then promotes the proliferation of collagen in the middle and late stages. Moreover, PRP can stimulate Act A and M1 polarization in the early stage, while inhibiting activin A (Act A) and inducing M2 polarization in the middle and late stages. In conclusion, this study demonstrates that PRP plays an important regulatory role in helping reduce UVB-induced acute skin tissue inflammation by adjusting macrophage polarization, which alleviates skin inflammation and stimulates collagen regeneration.

Analysis of Ultraviolet Radiation Wavelengths Causing Hardening and Reduced Elasticity of Collagen Gels In Vitro

Regular exposure of facial skin to sunlight promotes wrinkle formation; ultraviolet (UV) radiation causes the skin to harden and lose its elasticity. To study UV damage to the skin in vitro, a short-term in vitro photoaging model is required. Hence, the UV transmittance of excised human skin was measured. Changes in elasticity in the cheeks of humans of different ages were investigated. Moreover, changes in the hardness and elasticity of collagen gels following UV exposure were investigated. UV rays penetrated the upper layer of the dermis and UVA (330 nm) rays penetrated approximately 1.6 times farther than UVB (310 nm) rays. A correlation between age and lower cheek elasticity was observed. Upon exposure to UV rays, collagen gels hardened and their elasticity decreased; UVA rays exhibited a stronger effect than UVB rays. Wavelengths of 300–340 nm caused hardening and reduced elasticity of collagen gels; 330-nm radiation showed the most pronounced effect. These effects were not observed upon exposure to UV wavelengths over 350 nm. Investigating the UV-hardening mechanism of collagen showed increased tyrosine crosslinks (dityrosines) in the in vitro model of photodamage to collagen, suggesting that dityrosine formation contributes to hardening and reduced elasticity of collagen in photoaged skin.

Reversible Disruption of Neuronal Mitochondria by Ischemic and Traumatic Injury Revealed by Quantitative Two-Photon Imaging in the Neocortex of Anesthetized Mice

Mitochondria play a variety of functional roles in cortical neurons, from metabolic support and neuroprotection to the release of cytokines that trigger apoptosis. In dendrites, mitochondrial structure is closely linked to their function, and fragmentation (fission) of the normally elongated mitochondria indicates loss of their function under pathological conditions, such as stroke and brain trauma. Using <i>in vivo</i> two-photon microscopy in mouse brain, we quantified mitochondrial fragmentation in a full spectrum of cortical injuries, ranging from severe to mild. Severe global ischemic injury was induced by bilateral common carotid artery occlusion, whereas severe focal stroke injury was induced by Rose Bengal photosensitization. The moderate and mild traumatic injury was inflicted by focal laser lesion and by mild photo-damage, respectively. Dendritic and mitochondrial structural changes were tracked longitudinally using transgenic mice expressing fluorescent proteins localized either in cytosol or in mitochondrial matrix. In response to severe injury, mitochondrial fragmentation developed in parallel with dendritic damage signified by dendritic beading. Reconstruction from serial section electron microscopy confirmed mitochondrial fragmentation. Unlike dendritic beading, fragmentation spread beyond the injury core in focal stroke and focal laser lesion models. In moderate and mild injury, mitochondrial fragmentation was reversible with full recovery of structural integrity after 1–2 weeks. The transient fragmentation observed in the mild photo-damage model was associated with changes in dendritic spine density without any signs of dendritic damage. Our findings indicate that alterations in neuronal mitochondria structure are very sensitive to the tissue damage and can be reversible in ischemic and traumatic injuries. <b>SIGNIFICANCE STATEMENT</b> During ischemic stroke or brain trauma, mitochondria can either protect neurons by supplying ATP and adsorbing excessive Ca²⁺, or kill neurons by releasing proapoptotic factors. Mitochondrial function is tightly linked to their morphology: healthy mitochondria are thin and long; dysfunctional mitochondria are thick (swollen) and short (fragmented). To date, fragmentation of mitochondria was studied either in dissociated cultured neurons or in brain slices, but not in the intact living brain. Using real-time <i>in vivo</i> two-photon microscopy, we quantified mitochondrial fragmentation during acute pathological conditions that mimic severe, moderate, and mild brain injury. We demonstrated that alterations in neuronal mitochondria structural integrity can be reversible in traumatic and ischemic injuries, highlighting mitochondria as a potential target for therapeutic interventions.

Norbixin Protects Retinal Pigmented Epithelium Cells and Photoreceptors against A2E-Mediated Phototoxicity In Vitro and In Vivo.

The accumulation of N-retinylidene-N-retinylethanolamine (A2E, a toxic by-product of the visual pigment cycle) in the retinal pigment epithelium (RPE) is a major cause of visual impairment in the elderly. Photooxidation of A2E results in retinal pigment epithelium degeneration followed by that of associated photoreceptors. Present treatments rely on nutrient supplementation with antioxidants. 9’-cis-Norbixin (a natural diapocarotenoid, 97% purity) was prepared from Bixa orellana seeds. It was first evaluated in primary cultures of porcine retinal pigment epithelium cells challenged with A2E and illuminated with blue light, and it provided an improved photo-protection as compared with lutein or zeaxanthin. In Abca4-/- Rdh8-/- mice (a model of dry AMD), intravitreally-injected norbixin maintained the electroretinogram and protected photoreceptors against light damage. In a standard rat blue-light model of photodamage, norbixin was at least equally as active as phenyl-N-tert-butylnitrone, a free radical spin-trap. Chronic experiments performed with Abca4-/- Rdh8-/- mice treated orally for 3 months with norbixin showed a reduced A2E accumulation in the retina. Norbixin appears promising for developing an oral treatment of macular degeneration. A drug candidate (BIO201) with 9’-cis-norbixin as the active principle ingredient is under development, and its potential will be assessed in a forthcoming clinical trial.

Photodamage to the oxygen evolving complex of photosystem II by visible light.

Light damages photosynthetic machinery, primarily photosystem II (PSII), and it results in photoinhibition. A new photodamage model, the two-step photodamage model, suggests that photodamage to PSII initially occurs at the oxygen evolving complex (OEC) by light energy absorbed by manganese and that the PSII reaction center is subsequently damaged by light energy absorbed by photosynthetic pigments due to the limitation of electrons to the PSII reaction center. However, it is still uncertain whether this model is applicable to photodamage to PSII under visible light as manganese absorbs visible light only weakly. In the present study, we identified the initial site of photodamage to PSII upon illumination of visible light using PSII membrane fragments isolated from spinach leaves. When PSII samples were exposed to visible light in the presence of an exogenous electron acceptor, both PSII total activity and the PSII reaction centre activity declined due to photodamage. The supplemental addition of an electron donor to the PSII reaction centre alleviated the decline of the reaction centre activity but not the PSII total activity upon the light exposure. Our results demonstrate that visible light damages OEC prior to photodamage to the PSII reaction center, consistent with two-step photodamage model.

Effects of repetitive ultraviolet A radiation on the endocytosis and degradation of elastin by human skin fibroblasts

Objective To investigate the effects of repetitive ultraviolet A(UVA) radiation on the endocytosis and intracellular degradation of extracellular elastin by human dermal fibroblasts (HDFs), and to explore the mechanism responsible for elastin accumulation in photoaging skin. Methods Cultured HDFs were divided into two groups: repetitive UVA radiation group treated with UVA radiation (9.9 J/cm2) once a day for seven consecutive days to establish a chronic photodamage model, and blank control group receiving no treatment. For the verification of the model, flow cytometry was performed to detect cell cycle, and senescence-associated β-galactosidase staining to determine the degree of cell senescence. Fluorescent tracer technique and conjugated polymer-based fluorescence quenching technique were conducted to observe the endocytosis and intracellular degradation of extracellular elastin in culture media by HDFs in these groups. Results Compared with the blank control group, the repetitive UVA radiation group showed increased proportions of G1-phase cells and senescent cells, which confirmed the successful establishment of chronic photodamage model in the repetitive UVA radiation group. After coculture with elastin for 24, 48 and 72 hours, the endocytosis rate of elastin was 10.0%±1.4%, 27.8%±4.2% and 39.9%±4.1% respectively in the blank control group, 9.9%±1.6%, 28.3%±5.1% and 42.0%±5.7% respectively in the repetitive UVA radiation group, with no significant difference between the two groups at the three time points (all P>0.05). The percentage of cells showing intracellular degradation of extracellular elastin was significantly lower in the repetitive UVA radiation group than in the blank control group (4.2%±1.1% vs. 7.7%±0.9% at 24 hours, 16.5%±2.4% vs. 22.8%±1.8% at 48 hours, 26.7%±2.6% vs. 33.9%±3.1% at 72 hours, all P<0.05). Conclusions UVA radiation at 9.9 J/cm2 for 7 consecutive days can decrease the intracellular degradation of extracellular elastin by HDFs, but has no obvious effect on endocytosis of elastin. Key words: Fibroblasts; Skin aging; Ultraviolet rays; Elastin; Proteolysis; Endocytosis

Effect of sunlight transformed by luminophore-containing materials on cell functions in vitro and in vivo.

Effect of sunlight transformed by luminophore-containing materials on cell viability and functional state of the retina was assessed using the photodamage model. Exposure to the luminescent component of light improved viability of NIH 3T3 cells and promoted recovery of electric activity in rabbit retina after photodamage.

The Endogenous Protease Inhibitor TIMP-1 Mediates Protection and Recovery from Cutaneous Photodamage

UVB exposure is well known to induce skin photodamage and photoaging that correlates with qualitative and quantitative deterioration of the dermal extracellular matrix (ECM) because of the upregulation of matrix metalloproteinases (MMPs). Although inhibitory effects of tissue inhibitor of metalloproteinases (TIMPs) on most MMPs have been reported, the protective role of TIMP-1 against photodamage is poorly understood. To address this, TIMP-1 function was augmented or abolished in a human skin xenograft photodamage model after the confirmation of significantly diminished TIMP-1 expression both in photoaged and intrinsically aged skins. During a chronic UVB exposure regimen, pre-treatment with a lentiviral vector overexpressing TIMP-1 or concomitant administration of an anti-TIMP-1-neutralizing antibody (NAB) led to photoprotection or more severe photodamage, respectively. Overexpression of TIMP-1 resulted in significant inhibition of UVB-induced ECM degradation, as well as suppression of decreased skin elasticity and roughness, whereas the NAB-mediated inhibition of TIMP-1 had opposite effects. Furthermore, UVB-induced production of the pro-inflammatory cytokine, tumor necrosis factor α, was inhibited by TIMP-1 treatment of human keratinocytes. Taken together, these data shed light on the important role of TIMP-1 in protection and recovery from cutaneous photodamage because of its suppression of ECM degradation and inflammation.

Establishment of mus skin photo-damage model by 8-MOP plus UVA irradiation

To establish a simple and reliable animal model of skin photo-damage, 20 mice were treated with 8-MOP and exposed to UVA (UVA 320-400 nm) for 24 h. After irradiation, the structure of the epidermis and dermis, collagen fibers, elastic fibers were observed by using HE staining and Weigert technique and compared with the normal controls. The acanthosis and epidermis proliferation with accompanying hyperkeratosis and parakeratosis were observed. Inflammatory infiltration was noted in the dermis. The elastic fibers became coarse, irregularly arranged and clustered, with their number increased. The collagen fibers showed obvious degeneration and some amorphous materials could also be observed. The blood vessels were irregularly dilated and vascular walls were thickened, with infiltration of inflammatory cells. It is concluded that murine photodamage model can be quickly, conveniently and reliably established by means of 8-MOP/UVA.

Protection from photodamage by topical application of caffeine after ultraviolet irradiation

Characterization of mechanisms that can reverse residual damage from prior skin exposure to ultraviolet (UV) would be of considerable biological and therapeutic interest. Topical caffeine application to mouse skin that had previously been treated with UV has been shown to inhibit the subsequent development of squamous cell carcinomas. We used an established mouse photodamage model to investigate other possible effects of topical caffeine application after UV. SKH-1 hairless mice were treated with ultraviolet B (UVB) followed immediately by topical application of caffeine or vehicle three times weekly for 11 weeks. Caffeine applied topically after UV treatment resulted in a significant decrease in UV-induced skin roughness/transverse rhytides as assessed by treatment-blinded examiners. Histologically, topical caffeine application after a single dose of UVB more than doubled the number of apoptotic keratinocytes as evaluated by sunburn cell formation, caspase 3 cleavage and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) staining. A trend towards decreased solar elastosis was noted in the caffeine-treated group although this was not statistically significant. Other histological parameters including epidermal hyperplasia, solar elastosis and angiogenesis were increased in mice treated with UV but topical application of caffeine did not alter these particular UV effects. These findings support the concept that topical application of caffeine to mouse skin after UV irradiation promotes the deletion of DNA-damaged keratinocytes and may partially diminish photodamage as well as photocarcinogenesis.

Measurement of protection afforded by ultraviolet-absorbing window film using an in vitro model of photodamage

The effects of chronic sun damage including telangiectasias, solar lentigos, rhytides, enlarged pores, sagging skin, and pre-cancerous and cancerous growths are among the most common presenting complaints in a dermatologist's office. These changes are often worse on the driver's side of the face, emphasizing the role of UVA exposure received while driving in producing these changes. This study was undertaken to measure the ability of car window glass alone and in combination with ultraviolet (UV)-absorbing film to reduce UV-damage as measured using an established in vitro model of photoprotection. STUDY DESIGN MATERIALS AND METHODS: Using the 3T3 neutral red uptake photoprotection assay with solar simulating radiation (SSR) administered by a xenon arc solar simulator, we measured the photoprotection ability of auto glass, window film that filters UV radiation, and the combination of window film and auto glass. As measured by the 3T3 neutral red uptake photoprotection assay, auto glass reduced cell death from SSR by 29%, while window film reduced it 90%, and the combination of auto glass and film reduced cell death by 93%, when compared to unfiltered SSR. Window film that filters UV radiation results in dramatic reductions in cytotoxicity when measured by the neutral red uptake photoprotection assay. Widespread use of window film provides an ever-present barrier to ultraviolet A (UVA) exposure and could potentially reduce the detrimental effects of UVA, including photoaging, skin cancer, and ocular damage, such as cataracts. In addition, such film is essential for patients suffering from conditions sensitive to UV radiation, such as lupus erythematosis.