Ultraviolet B Exposure Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Mice by Expanding CD4Foxp3Regulatory T Cells.
J Am Heart Assoc. 2017 Aug 31 ;6(9). Epub 2017 Aug 31. PMID: 28860231
Tomohiro Hayashi, Naoto Sasaki, Tomoya Yamashita, Taiji Mizoguchi, Takuo Emoto, Hilman Zulkifli Amin, Keiko Yodoi, Takuya Matsumoto, Kazuyuki Kasahara, Naofumi Yoshida, Tokiko Tabata, Naoki Kitano, Atsushi Fukunaga, Chikako Nishigori, Yoshiyuki Rikitake, Ken-Ichi Hirata
BACKGROUND: Pathogenic immune responses are known to play an important role in abdominal aortic aneurysm (AAA) development. Ultraviolet B (UVB) irradiation has been demonstrated to have therapeutic potential not only for cutaneous diseases but also for systemic inflammatory diseases in mice by suppressing immunoinflammatory responses. We investigated the effect of UVB irradiation on experimental AAA.
METHODS AND RESULTS: We used an angiotensin II-induced AAA model in apolipoprotein E-deficient mice fed a high-cholesterol diet. Mice aged 10 weeks were irradiated with 5 kJ/mUVB once weekly for 6 weeks (UVB-irradiated, n=38; nonirradiated, n=42) and were euthanized for evaluation of AAA formation at 16 weeks. Overall, 93% of angiotensin II-infused mice developed AAA, with 60% mortality possibly because of aneurysm rupture. UVB irradiation significantly decreased the incidence (66%) and mortality (29%) of AAA (=0.004 and=0.006, respectively). UVB-irradiated mice had significantly smaller diameter AAA (=0.008) and fewer inflammatory cells in the aortic aneurysm tissue than nonirradiated mice, along with systemic expansion of CD4Foxp3regulatory T cells and decreased effector CD4CD44CD62LT cells in para-aortic lymph nodes. Genetic depletion of regulatory T cells abrogated these beneficial effects of UVB treatment, demonstrating a critical role of regulatory T cells.
CONCLUSIONS: Our data suggest that UVB-dependent expansion of regulatory T cells has beneficial effects on experimental AAA and may provide a novel strategy for the treatment of AAA.
Article Published Date : Aug 30, 2017
Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells.
Tumour Biol. 2017 Jun ;39(6):1010428317706216. PMID: 28618944
Yong Xin, Qian Huang, Pei Zhang, Wen Wen Guo, Long Zhen Zhang, Guan Jiang
Photodynamic therapy is widely used in the clinical treatment of tumors, especially skin cancers. It has been reported that the photosensitizer curcumin, in combination with ultraviolet radiation B, induces HaCaT cell apoptosis, and this effect may be due to the activation of caspase pathways. In this study, we examined the photodynamic effects of demethoxycurcumin, a more stable analogue of curcumin, to determine whether it could induce apoptosis in skin cancer cells. We investigated the effects of a combination of ultraviolet radiation B and demethoxycurcumin on apoptotic cell death in A431 and HaCaT cells and determined the molecular mechanism of action. Our results showed increased apoptosis with a combination of ultraviolet radiation B with demethoxycurcumin, as compared to ultraviolet radiation B or demethoxycurcumin alone. The combination of ultraviolet radiation B irradiation with demethoxycurcumin synergistically induced apoptotic cell death in A431 and HaCaT cells through activation of p53 and caspase pathways, as well as through upregulation of Bax and p-p65 expression and downregulation of Bcl-2, Mcl-1, and nuclear factor-κB expression. In addition, we found that reactive oxygen species significantly increased with treatment, and mitochondrial membrane potential depolarization was remarkably enhanced. In conclusion, our data indicate that demethoxycurcumin may be a promising photosensitizer for use in photodynamic therapy to induce apoptosis in skin cancer cells.
Article Published Date : May 31, 2017
Enhancement of Vitamin D Metabolites in the Eye Following Vitamin D3 Supplementation and UV-B Irradiation.
Curr Eye Res. 2012 May 25. Epub 2012 May 25. PMID: 22632164
Yanping Lin, John L Ubels, Mark P Schotanus, Zhaohong Yin, Victorina Pintea, Bruce D Hammock, Mitchell A Watsky
Department of Entomology&Cancer Center, University of California , Davis, CA , USA.
Purpose: This study was designed to measure vitamin D metabolites in the aqueous and vitreous humor and in tear fluid, and to determine if dietary vitamin D3 supplementation affects these levels. We also determined if the corneal epithelium can synthesize vitamin D following UV-B exposure. Methods: Rabbits were fed a control or vitamin D3 supplemented diet. Pilocarpine-stimulated tear fluid was collected and aqueous and vitreous humor were drawn from enucleated eyes. Plasma vitamin D was also measured. To test for epithelial vitamin D synthesis, a human corneal limbal epithelial cell line was irradiated with two doses of UV-B (10 and 20 mJ/cm(2)/day for 3 days) and vitamin D was measured in control or 7-dehydrocholesterol treated culture medium. Measurements were made using mass spectroscopy. Results: 25(OH)-vitamin D3 and 24,25(OH)(2)-vitamin D3 increased significantly following D3 supplementation in all samples except vitreous humor. Tear fluid and aqueous humor had small but detectable 1,25(OH)(2)-vitamin D3 levels. Vitamin D2 metabolites were observed in all samples. Vitamin D3 levels were below the detection limit for all samples. Minimal vitamin D3 metabolites were observed in control and UV-B-irradiated epithelial culture medium except following 7-dehydrocholesterol treatment, which resulted in a UV-B-dose dependent increase in vitamin D3, 25(OH)-vitamin D3 and 24,25(OH)(2)-vitamin D3. Conclusions: There are measurable concentrations of vitamin D metabolites in tear fluid and aqueous and vitreous humor, and oral vitamin D supplementation affects vitamin D metabolite concentrations in the anterior segment of the eye. In addition, the UV exposure results lead us to conclude that corneal epithelial cells are likely capable of synthesizing vitamin D3 metabolites in the presence of 7-dehydrocholesterol following UV-B exposure.
Article Published Date : May 25, 2012
Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion.
Behav Neurosci. 2012 Feb ;126(1):196-203. Epub 2011 Dec 26. PMID: 22201280
Mirjam Münch, Friedrich Linhart, Apiparn Borisuit, Susanne M Jaeggi, Jean-Louis Scartezzini
Solar Energy and Building Physics Laboratory, Swiss Federal Institute of Technology, Lausanne.
In sighted humans, light intensity, timing, exposure duration, and spectral composition of light are important to entrain the endogenous circadian pacemaker to the 24-h day-night cycle. We tested the impact of two realistic office lighting conditions during the afternoon on subjective sleepiness, hormonal secretion, and cognitive performance in the early evening hours. Twenty-nine young subjects came twice and spent 8 h (12:00-20:00) in our laboratory, where they were exposed for 6 h to either artificial light (AL) or to mainly daylight (DL). In the early evening, we assessed their salivary cortisol and melatonin secretion, subjective sleepiness, and cognitive performance (n-back test) under dim light conditions. Subjects felt significantly more alert at the beginning of the evening after the DL condition, and they became sleepier at the end of the evening after the AL condition. For cognitive performance we found a significant interaction between light conditions, mental load (2- or 3-back task) and the order of light administration. On their first evening, subjects performed with similar accuracy after both light conditions, but on their second evening, subjects performed significantly more accurately after the DL in both n-back versions and committed fewer false alarms in the 2-back task compared to the AL group. Lower sleepiness in the evening was significantly correlated with better cognitive performance (p<.05). In summary, even short-term lighting conditions during the afternoon had an impact on cognitive task performance in the evening. This rapid effect was only distinguishable on the second day of training, when a difficult task had been sufficiently practiced.
Article Published Date : Feb 01, 2012
The deceptive nature of UVA tanning versus the modest protective effects of UVB tanning on human skin.
Pigment Cell Melanoma Res. 2011 Feb ;24(1):136-47. Epub 2010 Oct 6. PMID: 20979596
Yoshinori Miyamura, Sergio G Coelho, Kathrin Schlenz, Jan Batzer, Christoph Smuda, Wonseon Choi, Michaela Brenner, Thierry Passeron, Guofeng Zhang, Ludger Kolbe, Rainer Wolber, Vincent J Hearing
Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD, USA.
The relationship between human skin pigmentation and protection from ultraviolet (UV) radiation is an important element underlying differences in skin carcinogenesis rates. The association between UV damage and the risk of skin cancer is clear, yet a strategic balance in exposure to UV needs to be met. Dark skin is protected from UV-induced DNA damage significantly more than light skin owing to the constitutively higher pigmentation, but an as yet unresolved and important question is what photoprotective benefit, if any, is afforded by facultative pigmentation (i.e. a tan induced by UV exposure). To address that and to compare the effects of various wavelengths of UV, we repetitively exposed human skin to suberythemal doses of UVA and/or UVB over 2 weeks after which a challenge dose of UVA and UVB was given. Although visual skin pigmentation (tanning) elicited by different UV exposure protocols was similar, the melanin content and UV-protective effects against DNA damage in UVB-tanned skin (but not in UVA-tanned skin) were significantly higher. UVA-induced tans seem to result from the photooxidation of existing melanin and its precursors with some redistribution of pigment granules, while UVB stimulates melanocytes to up-regulate melanin synthesis and increases pigmentation coverage, effects that are synergistically stimulated in UVA and UVB-exposed skin. Thus, UVA tanning contributes essentially no photoprotection, although all types of UV-induced tanning result in DNA and cellular damage, which can eventually lead to photocarcinogenesis.
Article Published Date : Feb 01, 2011
Danshensu Decreases UVB-Induced Corneal Inflammation in an Experimental Mouse Model via Oral Administration.
Curr Eye Res. 2018 01;43(1):27-34
Authors: Teng MC, Wu PC, Lin SP, Wu CY, Wang PH, Chen CT, Chen BY
BACKGROUND: Danshensu is a bioactive constituent of Salvia miltiorrhiza, a plant commonly used in traditional Chinese medicine. In this study, we investigated the pharmacological efficacy of sodium danshensu, or named salvianic acid A sodium (SAS) on ultraviolet B (UVB)-mediated corneal inflammatory injury in mice.
METHODS: Albino mice were divided into one blank control group, and three UVB radiation groups, i.e. SAS-untreated group, and prophylactic treatment groups with SAS at 1 and 10 mg/kg via oral administration. The structure integrity and inflammatory changes of cornea were assessed by surface evaluation of smoothness, topographic distortion, opacity, lissamine green staining, and histologic tissue staining. The inflammatory cytokines was measured by bead-based ELISA assays.
RESULTS: Prophylactic treatment of SAS significantly inhibited pathologic changes, improved tissue structural integrity, and reduced inflammatory injury in the cornea after UVB exposure. Dosing with SAS treatment attenuated the incidence rate of leukocyte influx by inhibit increase of interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1, and tumor necrosis factor-α. Treatment with 10 mg/kg SAS was more effective in preventing the onset of corneal damage than that with 1 mg/kg SAS.
CONCLUSIONS: These results indicate that SAS exhibit the pharmacological efficacy on corneal protection through its inhibition of UVB induced photodamage and subsequently inflammatory injury in vivo.
PMID: 29111819 [PubMed - indexed for MEDLINE]