Allergic Potential & Molecular Mechanism of Skin Sensitization of Cinnamaldehyde Under Environmental UVB Exposure.

Fragrance, a key ingredient in cosmetics, often triggers skin allergy causes rashes, itching, dryness, and cracked or scaly skin. Cinnamaldehyde (CA), derived from the bark of the cinnamon tree, used as a fragrance and is a moderate skin sensitizer. CA exhibits strong UVB absorption, its allergic potential and the molecular mechanisms underlying skin sensitization under UVB exposure remain largely unexplored. To investigate the allergic potential and molecular mechanisms of CA-induced skin sensitization under ambient UVB radiation, we employed various alternative in-silico, in-chemico and in-vitro tools. CA under ambient UVB isomerizes from trans to cis CA after 1hr of exposure. Furthermore, DPRA assay and docking with simulation studies demonstrated the enhanced allergic potential of cis-CA. Additionally, our study evaluated intracellular ROS levels and the expression of Nrf2, Catalase, and MMP-2, and 9 in KeratinoSens cells, showing significant upregulation under UVB exposure in the presence of CA. Moreover, our findings indicate that CA activates THP-1 cells co-stimulatory surface marker (CD86) via the activation of intracellular ROS, phagocytosis, and genes of the TLR4 pathway. These insights into the mechanisms uncovered by our study are crucial for managing triggers of allergic skin diseases caused by fragrance use and concurrent exposure to environmental UVB/sunlight.

Succinylated Type I Collagen Regulates Ferroptosis to Attenuate Skin Photoaging.

During the process of photoaging in the skin, Succinylated type I collagen has a significant effect on reversing the damage caused by UVB radiation, with the regulation of cellular ferroptosis being one of its important pathophysiological mechanisms. Specifically, Succinylated type I collagen reduces the expression of key cell cycle regulators P16, P21, and P53, as well as the ferroptosis-related factor Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), induced by UVB radiation in cells and tissues. Meanwhile, it increases the expression of key factors Glutathione Peroxidase 4 (GPX4) and Solute Carrier Family 7 Member 11 (SLC7A11), which inhibit ferroptosis. Additionally, our study also reveals the impact of Succinylated type I collagen on the levels of malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) in cells and tissues, directly affecting the cells' ability to cope with oxidative stress. This further suggests that Succinylated type I collagen may improve skin photoaging through various pathways, including regulating ferroptosis, antioxidation, promoting collagen synthesis, protecting the skin barrier, reducing pigmentation, and inhibiting inflammatory responses, contributing to maintaining healthy and youthful skin.

Butin Protects Keratinocytes From Particulate Matter 2.5 and Ultraviolet B-Mediated Damages.

BACKGROUND: Butin is a naturally occurring compound with a wide range of medicinal properties, including anti-inflammatory, anti-arthritic, and antioxidant properties. Particulate matter 2.5 (PM2.5) and ultraviolet B (UVB) radiation contribute to skin cell damage via the induction of oxidative stress. METHODS: This study sought to assess the protective effects of butin against damage triggered by PM2.5 and UVB in human HaCaT keratinocytes. Assessments were performed to evaluate cell viability, apoptosis, and cellular component damage. RESULTS: Butin exhibited its protective ability via the inhibition of PM2.5-induced reactive oxygen species generation, lipid peroxidation, DNA damage, protein carbonylation, and mitochondrial damage. Butin reduced the PM2.5-induced c-Fos and phospho-c-Jun protein levels as well as mitogen-activated protein kinase. Furthermore, butin mitigated PM2.5- and UVB-induced apoptosis. CONCLUSION: Butin had the potential as a pharmaceutical candidate for treating skin damage caused by PM2.5 and UVB exposure.

Ultraviolet radiation thin film dosimetry: A review of properties and applications.

Spectroradiometry, radiometry, and dosimetry are employed for the measurement of ultraviolet radiation (UVR) irradiance and non-ionizing exposure. Different types of UVR dosimeter have been developed for measuring personal and environmental UVR exposures since film dosimetry was pioneered in the 1970s. An important type of dosimeter is the thin film variant, which contains materials that undergo changes in optical absorbance when exposed to UVR. These changes can be measured at a specific wavelength using a spectrophotometer. Thin film dosimeters allow UVR exposure measurements on humans at various body sites during daily activities, as well as on plants, animals, and any sites of interest when utilized in a field environment. This review examines the properties and applications of five types of thin film UVR dosimeter that have different dynamic exposure limits and spectral responses. Polysulphone, with a spectral response approximating the human erythema action spectrum, was one of the first materials employed in thin film form for the measurement of UVR exposures up to 1 day, and up to 6 days with an extended dynamic range filter. Polyphenylene oxide has been characterized and employed for personal UVR exposure measurements up to approximately four summer days and has also been used for long-term underwater UVR exposures. Phenothiazine and 8-methoxypsoralen have been reported as suitable for the measurement of longer wavelength UVA exposures. Finally, polyvinyl chloride with an extended dynamic exposure range of over 3 weeks has been shown to have predominantly a spectral response in the UVB and extending up to 340 nm.

FUNDC1-mediated mitophagy regulates photodamage independently of the PINK1/Parkin-dependent pathway.

BACKGROUND: Ultraviolet B(UVB) triggers a pro-survival response through mitophagy, but the role of FUNDC1-mediated mitophagy in photodamaged skin remains unexplored. OBJECTIVES: To clarify the function of mitophagy in UVB-induced photodamaged skin. METHODS: To investigate the role of FUNDC1-mediated mitophagy in UVB-induced mitochondrial damage and cell apoptosis, FUNDC1 knockdown in C57BL/6 mice was performed using adeno-associated virus. Additionally, FUNDC1 overexpression and knockdown in HaCaT cells were conducted using lentivirus. A comprehensive analysis was conducted on a panel of human sun-exposed skin samples, alongside control samples, to assess the expression levels of FUNDC1. RESULTS: In UVB-induced C57BL/6 mice, the dorsal skin showed photodamage including erythema, scaling, erosion, and scabs. The expression levels of PINK1, Parkin, and BNIP3 did not show significant changes, while FUNDC1 expression consistently declined along with LC3B. Cytochrome C, Bax, and cleaved-caspase3 were upregulated, while Bcl2 was downregulated. UVB-induced HaCaT cells showed mitochondrial damage, accompanied by FUNDC1 downregulation and BNIP3 upregulation, while PINK1 and Parkin showed no significant changes. FUNDC1 overexpression led to an increase in mtROS and a decrease in mitochondrial membrane potential and ATP levels, indicating complete mitochondrial clearance and exacerbated cell death. FUNDC1 knockdown protected against UVB-induced photodamage in mice and mitigated mitochondrial damage and apoptosis in HaCaT cells by activating compensatory PINK1/Parkin-dependent mitophagy, which was evidenced by upregulation of PINK1 and Bcl2 and downregulation of Bax. In human sun-exposed skin samples, there was a decrease in the number of FUNDC1+ cells compared with non-sun-exposed controls. CONCLUSIONS: FUNDC1-mediated mitophagy regulates skin photodamage and provides a novel mechanism for resisting photodamage, presenting a potential target for future therapeutic interventions.

How Metarhizium robertsii's mycelial consciousness gets its conidia Zen-ready for stress.

This memoir takes a whimsical ride through my professional adventures, spotlighting my fungal stress research on the insect-pathogenic fungus Metarhizium robertsii, which transformed many of my wildest dreams into reality. Imagine the magic of fungi meeting science and me, a happy researcher, arriving at Utah State University ready to dive deep into studies with the legendary insect pathologist, my advisor Donald W. Roberts, and my co-advisor Anne J. Anderson. From my very first "Aha!" moment in the lab, I plunged into a vortex of discovery, turning out research like a mycelium on a mission. Who knew 18 h/day, seven days a week, could be so exhilarating? I was fueled by an insatiable curiosity, boundless creativity, and a perhaps slightly alarming level of motivation. Years later, I managed to bring my grandest vision to life: the International Symposium on Fungal Stress-ISFUS. This groundbreaking event has attracted 162 esteemed speakers from 29 countries to Brazil, proving that fungi can be both fun and globally fascinating. ISFUS is celebrating its fifth edition in 2024, a decade after its 2014 debut.

UV-B increases active phytochrome B to suppress thermomorphogenesis and enhance UV-B stress tolerance at high temperatures.

Plants respond to small increases in ambient temperature by changing their architecture, a response collectively termed thermomorphogenesis. Thermomorphogenesis is considered to attenuate the damage caused by potentially harmful high-temperature conditions, and multiple environmental factors can modulate this process. Among these factors, ultraviolet-B (UV-B) light has been shown to strongly suppress this response. However, the molecular mechanisms through which it regulates thermomorphogenesis and the physiological roles of the UV-B-mediated suppression of thermomorphogenesis remain poorly understood. Here, we show that UV-B inhibits thermomorphogenesis through the UVR8-COP1-phyB/HFR1 signaling module. We found that cop1 mutants maintain high levels of active phyB at high temperatures. Extensive genetic analyses revealed that the increased phyB, HFR1, and CRY1 in cop1 mutants redundantly reduce both the level and activity of a key positive regulator in thermomorphogenesis, PIF4, thereby repressing this growth response. Additionally, we found that UV-B light increases phyB stability and its photobody number through the inactivation of COP1. The UV-B-stabilized active phyB, together with HFR1, inhibits thermomorphogenesis by interfering with PIF4. We further show that the increased active phyB enhances UV-B tolerance by activating flavonoid biosynthesis and inhibiting thermomorphogenic growth. Taken together, our study demonstrates that UV-B increases the levels of active phyB and HFR1 by inhibiting COP1 to suppress PIF4-mediated growth responses, which is essential for plant tolerance to UV-B stress at high temperatures.

Panax ginseng extract prevents UVB-induced skin photodamage by modulating VMP1-mediated ER stress.

BACKGROUND: The endoplasmic reticulum (ER) stress is a crucial toxic signaling event triggered by chronic exposure to Ultraviolet B radiation (UVB), which significantly exacerbate photodamage responses in the irradiated skin. Therefore, the identification of agents capable of inhibiting ER stress could serve as a promising therapeutic strategy for addressing the unmet clinical needs in the treatment of UVB-induced photodamage. METHODS: A UVB-irradiated mouse model was used and topical administration of Panax ginseng extract was carried out for a duration of 9 weeks. Vitamin E was used as a positive control. After 9 weeks of administration, the skin appearance, epidermal hyperplasia, infiltration of inflammatory cells, apoptosis, and collagen content were measured. The keratinocytes were irradiated with 6 mJ/cm2 UVB to establish an in vitro model. The levels of ER stress and apoptosis were investigated both in vivo and in vitro using qRT-PCR, immunoblotting, and immunofluorescence. RESULTS: Among the 14 extracts derived from 13 distinct plant species that were screened, Panax ginseng, Prunus mume, and Camellia japonica showed inhibitory effect on UVB-induced ER stress. Notably, Panax ginseng effectively inhibits collagen degradation and apoptosis in both irradiated keratinocytes and Balb/C mice skin. Furthermore, the silencing of VMP1 significantly impeded the cellular protective effect of Panax ginseng extract on UVB-irradiated keratinocytes, indicating that Panax ginseng exerts its protective effects through targeted promotion of VMP1. CONCLUSION: Our data suggest that Panax ginseng extract possess a therapeutical effect on UVB radiation-induced photodamage by promoting VMP1-mediated inhibition of ER stress.

UV light and the ocular lens: a review of exposure models and resulting biomolecular changes.

UV light is known to cause damage to biomolecules in living tissue. Tissues of the eye that play highly specialised roles in forming our sense of sight are uniquely exposed to light of all wavelengths. While these tissues have evolved protective mechanisms to resist damage from UV wavelengths, prolonged exposure is thought to lead to pathological changes. In the lens, UV light exposure is a risk factor for the development of cataract, which is a condition that is characterised by opacity that impairs its function as a focusing element in the eye. Cataract can affect spatially distinct regions of the lens. Age-related nuclear cataract is the most prevalent form of cataract and is strongly associated with oxidative stress and a decrease in the antioxidant capacity of the central lens region. Since UV light can generate reactive oxygen species to induce oxidative stress, its effects on lens structure, transparency, and biochemistry have been extensively investigated in animal models in order to better understand human cataract aetiology. A review of the different light exposure models and the advances in mechanistic understanding gained from these models is presented.

IRE1α regulates ROS and immune responses after UVB irradiation.

Objective: UV irradiation of the skin induces photo damage and generates cytotoxic intracellular reactive oxygen species (ROS), activating the unfolded protein response (UPR) to adapt or reduce these UVB-mediated damages. This study was designed to understand the role of the UPR mediator IRE1α in the antioxidant response following UVB irradiation of mouse skin and keratinocytes. Methods: We used mice with an epidermal deletion of IRE1α and primary mouse keratinocytes to examine effects of UV on different parameters of the antioxidant response in the presence and absence of functional IRE1α. Results: In the absence of IRE1α, PERK activity and protein levels are significantly compromised following UVB irradiation. Additionally, the loss of IRE1α suppressed phosphorylation of the PERK target, nuclear factor erythroid-2-related factor 2 (NRF2), and NRF2-dependent antioxidant gene expression after UVB irradiation. Interestingly, IRE1α-deficient keratinocytes exhibit elevated basal ROS levels, while a robust ROS induction upon UVB exposure is abolished. Because UVB-induced ROS plays an essential role in regulating skin inflammation, we analyzed recruited immune cell populations and the expression of pro-inflammatory cytokines, Il-6 and Tnfα in mice with epidermally-targeted deletion of Ire1α. Following UVB irradiation, there was significantly less recruitment of neutrophils and leukocytes and reduced expression of pro-inflammatory cytokine genes in the skin of mice lacking IRE1α. Furthermore, keratinocyte proliferation was also significantly reduced after chronic UVB exposure in the skin of these mice. Conclusions: Collectively, our findings indicate that IRE1α is essential for basal and UVB-induced oxidative stress response, UV-induced skin immune responses, and keratinocyte proliferation. Significance: These findings shed new light on the protective function of IRE1α in the response to UV. IRE1α plays an important role in the regulation of ROS, PERK stability, and antioxidant gene expression in response to UVB in mouse keratinocytes and epidermis.

Langerhans cells orchestrate apoptosis of DNA-damaged keratinocytes upon high-dose UVB skin exposure.

Ultraviolet (UV) irradiation of the skin causes mutations that can promote the development of melanoma and nonmelanoma skin cancer. High-dose UVB exposure triggers a vigorous skin reaction characterized by inflammation resulting in acute sunburn. This response includes the formation of sunburn cells and keratinocytes (KC) undergoing programmed cell death (apoptosis) when repair mechanisms of DNA damage are inadequate. The primary objective of this research was to clarify the involvement of Langerhans cells (LC) in the development of acute sunburn following intense UVB skin irradiation. To address this, we subjected the dorsal skin of mice to a single high-dose UVB exposure and analyzed the immediate immune response occurring within the skin tissue. Acute sunburn triggered an activation of LC, coinciding with a rapid influx of neutrophils that produced TNF-α. Furthermore, our investigation unveiled a marked increase in DNA-damaged KC and the subsequent induction of apoptosis in these cells. Importantly, we demonstrate a crucial link between the inflammatory cascade, the initiation of apoptosis in DNA-damaged KC, and the presence of LC in the skin. LC were observed to modulate the chemokine response in the skin following exposure to UVB, thereby affecting the trafficking of neutrophils. Skin lacking LC revealed diminished inflammation, contained fewer TNF-α-producing neutrophils, and due to the prevention of apoptosis induction, a lingering population of DNA-damaged KC, presumably carrying the risk of enduring genomic alterations. In summary, our results underscore the pivotal role of LC in preserving the homeostasis of UVB-irradiated skin. These findings contribute to a deeper understanding of the intricate mechanisms underlying acute sunburn responses and their implications for UV-induced skin cancer.

The preventive effects of natural plant compound carvacrol against combined UVA and UVB-induced endoplasmic reticulum stress in skin damage of rats.

The skin is constantly exposed to a variety of environmental stressors, including ultraviolet (UV) radiation. Exposure of the skin to UV radiation causes a number of detrimental biological damages such as endoplasmic reticulum (ER) stress. The ER stress response is a cytoprotective mechanism that maintains homeostasis of the ER by increasing the capacity of the ER against the accumulation of unfolded proteins in the ER. Carvacrol (CRV) is a monoterpenoid phenol found in essential oils with antimicrobial and anti-inflammatory activities. We investigated for the first time in the literature the potential protective role of CRV against combined UVA and UVB-induced skin damage by targeting the ER stress pathway in a rat model. For this purpose, expressions of Grp78, Perk, Atf6, Ire-1, Chop, Xbp1, Casp12, elF2α, and Traf2 genes related to ER stress were analyzed by RT-PCR and protein expression levels of GRP78, ATF6, CHOP, and XBP1 were determined by ELISA assay in tissue sections taken from the back of the rats. As a result of analysis, it was seen that the expression levels of aforementioned ER stress genes increased significantly in the UVA + UVB irradiated group compared to the control group, while their expression levels decreased markedly by supplementation of CRV in UVA + UVB + CRV group. With regard to expressions of foregoing proteins, their levels escalated notably with UVA + UVB application and decreased markedly by CRV supplementation. In conclusion, present study revealed that CRV ameliorates UVA + UVB-induced ER stress via reducing the expression of mRNA as well as proteins involved in the unfolded protein response (UPR) pathway and inducing apoptosis as evidenced from high Caspase12 level.

Chronic UVB exposure induces hepatic injury in mice: Mechanistic insights from integrated multi-omics.

Chronic UVB exposure poses a significant threat to both skin and visceral health. In recent years, the adverse role of chronic UVB exposure in liver health has been suggested but not fully elucidated. This study aims to comprehensively investigate the effects of chronic UVB exposure on liver health in male SKH-1 hairless mice and clarify potential mechanisms through multi-omics approaches. The findings suggested that 10-week chronic skin exposure to UVB not only triggers hepatic inflammation and oxidative stress but also, more importantly, results in lipid metabolism abnormalities in the liver. Hepatic transcriptomic analysis revealed significant alterations in various signaling pathways and physiological processes associated with inflammation, oxidative stress, and lipid metabolism. Further lipidomic analysis illustrated significant changes in the metabolism of glycerolipids, sphingolipids, and glycerophospholipids in the liver following chronic UVB exposure. The 16S rRNA sequencing analysis indicated that chronic UVB exposure disrupts the structure and function of the microbiota. In search of potential mechanisms used by the microbiome to regulate the hepatic disease morphology, we filtered mouse fecal supernatants and cultured the supernatants with HepG2 cells. Fecal supernatant from UVB-exposed mice induced increased secretion of the inflammatory cytokine IL-8, accumulation of MDA, reduced SOD activity, and decreased lipid content in normal hepatic cells. In summary, skin chronic exposure to UVB induces multiple liver injuries and gut microbiota dysbiosis in mice and gut microbiota metabolites may be one of the contributing factors to hepatic injury caused by chronic UVB exposure. These discoveries deepen the comprehension of the health risks associated with chronic UVB exposure.

Adapting the Goeckerman Regimen for Psoriasis Treatment in Kenya: A Case Study of Successful Management in a Resource-Limited Setting.

Introduction:  Goeckerman therapy, which combines ultraviolet B (UVB) light with crude coal tar (CCT), remains highly effective for moderate-to-severe psoriasis. While it is rarely still used in the USA as effective biotherapeutics have become more readily available, it offers an alternative therapy in developing countries with limited access to newer medications. Moi Teaching & Referral Hospital (MTRH) in Eldoret, Kenya, in collaboration with UCSF, developed a modified Goeckerman regimen suitable for local healthcare needs, condensing the treatment into an intensive two-week program. Case Report:  A 55-year-old female with erythrodermic psoriasis traveled 350 kilometers to MTRH. After the diagnosis was confirmed, she underwent a nine-day inpatient treatment with narrow-band UVB phototherapy and topical medications under occlusion as a modified Goeckerman regimen. Response to Treatment:  Significant improvement was observed within three days, with full recovery in ten days. Follow-up one month later showed no active lesions, and her psoriasis remained controlled for four months with topical treatments. Conclusion:  The modified Goeckerman regimen at MTRH, in collaboration with UCSF, effectively treated severe psoriasis in a challenging healthcare context. This case highlights the potential for adapting established treatments to improve patient outcomes in developing countries with limited access to systemic therapies.

Pilose Antler Protein Relieves UVB-Induced HaCaT Cells and Skin Damage.

Extended exposure to UVB (280-315 nm) radiation results in oxidative damage and inflammation of the skin. Previous research has demonstrated that pilose antler extracts have strong anti-inflammatory properties and possess antioxidant effects. This study aimed to elucidate the mechanism of pilose antler protein in repairing photodamage caused by UVB radiation in HaCaT cells and ICR mice. Pilose antler protein (PAP) was found to increase the expression of type I collagen and hyaluronic acid in HaCaT cells under UVB irradiation while also inhibiting reactive oxygen species (ROS) production and oxidative stress in vitro. In vivo, the topical application of pilose antler protein effectively attenuated UVB-induced skin damage in ICR mice by reducing interleukin-1ß (IL-ß), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) and inhibiting skin inflammation while alleviating UVB-induced oxidative stress. It was shown that pilose antler protein repaired UVB-induced photodamage through the MAPK and TGF-ß/Smad pathways.

BRAF Inhibition and UVB Light Synergistically Promote Mus musculus Papillomavirus 1-Induced Skin Tumorigenesis.

The development of keratinocytic skin tumors, presumably attributable to paradoxical activation of the MAPK pathway, represents a relevant side effect of targeted therapies with BRAF inhibitors (BRAFis). The role of cutaneous papillomavirus infection in BRAFi-associated skin carcinogenesis, however, is still inconclusive. Employing the Mus musculus papillomavirus 1 (MmuPV1) skin infection model, the impact of BRAFis and UVB exposure on papillomavirus induced skin tumorigenesis was investigated in immunocompetent FVB/NCrl mice. Systemic BRAF inhibition in combination with UVB light induced skin tumors in 62% of the MmuPV1-infected animals. In contrast, significantly fewer tumors were observed in the absence of either BRAF inhibition, UVB irradiation or virus infection, as demonstrated by lesional outgrowth in 20%, 5% and 0% of the mice, respectively. Combinatory exposure to BRAFis and UVB favored productive viral infection, which was shown by high numbers of MmuPV1 genome copies and E1^E4 spliced transcripts and an abundance of E6/E7 oncogene mRNA and viral capsid proteins. BRAF inhibition, but not viral infection or UVB light, activated ERK1/2, whereas γH2AX expression, inducible by UVB light, remained unaltered by BRAFis. These results provide experimental evidence that BRAF inhibition and UVB irradiation synergistically promote MmuPV1-induced skin tumor development in vivo. This indicates an alternative pathway by which papillomavirus skin infection may contribute to BRAFi-associated skin tumorigenesis.

Enhancing ocular protection against UVB: The role of irigenin in modulating oxidative stress and apoptotic pathways In Vivo.

Oxidative damage contributes to age-related macular degeneration. Irigenin possesses diverse pharmacologic properties, including antioxidative and antiapoptotic effects. Our in vivo experiments indicated that irigenin mitigates UVB-induced histopathologic changes and oxidative DNA damage. Histologic analyses and TUNEL staining revealed that this compound dose-dependently ameliorated UVB-induced retinal damage and apoptosis. Furthermore, irigenin substantially reduced the level of 8-hydroxyguanosine, a biomarker of UVB-induced oxidative DNA damage. We further explored the molecular mechanisms that mediate the protective effects of irigenin. Our findings suggested that UVB-induced generation of ROS disrupts the stability of the mitochondrial membrane, activating intrinsic apoptotic pathways; the underlying mechanisms include the release of cytochrome c, activation of caspase-9 and caspase-3, and subsequent degradation of PARP-1. Notably, irigenin reversed mitochondrial disruption and apoptosis. It also modulated the Bax and Bcl-2 expression but influenced the mitochondrial apoptotic pathways. Our study highlights the role of the Nrf2 pathway in mitigating the effects of oxidative stress. We found that UVB exposure downregulated, but irigenin treatment upregulated the expression of Nrf2 and antioxidant enzymes. Therefore, irigenin activates the Nrf2 pathway to address oxidative stress. In conclusion, irigenin exhibits protective effects against UVB-induced ocular damage, evidenced by the diminution of histological alterations. It mitigates oxidative DNA damage and apoptosis in the retinal tissues by modulating the intrinsic apoptotic pathways and the AIF mechanisms. Furthermore, irigenin effectively reduces lipid peroxidation, enhancing the activity of antioxidant enzymes by stimulating the Nrf2 pathway. This protective mechanism underscores the potential benefit of irigenin in combating UVB-mediated ocular damage.