Yurika Yamate

Intercellular pathway through hyaluronic acid in UVB-induced inflammation.

Ultraviolet B (UVB) radiation induces inflammation in the skin specifically at the site of exposure. We unexpectedly found that UVB‐induced inflammation was not induced in gp91phox‐depleted mice. To test whether gp91phox is directly involved in UVB‐induced inflammation, neutrophil‐ and hyaluronic acid–depleted mice were also irradiated and examined for their response. Hyaluronic acid–depleted mice showed strongly inhibited UVB‐induced inflammation, but the neutrophil‐depleted mice did not exhibit any suppressed UVB‐induced inflammation. To elucidate the pathway by which UVB irradiation induced inflammation, we examined the expression of nucleotide‐binding domain, leucine‐rich‐containing family, pyrin domain‐containing‐3 (NLRP3) and caspase‐1 in the mouse skin. An increase in the expression of NLRP3 and caspase‐1 was seen following the UVB irradiation of C57BL mice; however, the UVB‐irradiated gp91phox‐knockout (gp91phox−/−) mice did not have this increase in expression. Furthermore, the plasma IL‐1β level increased after the UVB irradiation in C57BL mice, but there was no change in the gp91phox−/− mice. These results clearly indicate that nicotinamide adenine dinucleotide phosphate oxidase is activated by gp91phox, which is expressed on the surface in response to the increased expression of hyaluronic acid induced by UVB irradiation, and as result, the generation of reactive oxygen species (ROS) increases. This ROS activate NLRP3, and NLRP3 leads to the production of caspase‐1, which subsequently increases IL‐1β, thereby finally inducing inflammation. It is thought that this system may play an important role in the damage and ageing of skin, and further studies are necessary to confirm these finding.

Tranexamic acid suppresses ultraviolet B eye irradiation-induced melanocyte activation by decreasing the levels of prohormone convertase 2 and alpha-melanocyte-stimulating hormone.

Tranexamic acid (trans‐4‐aminomethylcyclohexanecarboxylic acid) is a medicinal amino acid used in skin whitening care. This study examined the effects of tranexamic acid on the melanocyte activation of the skin induced by an ultraviolet (UV) B eye irradiation.

Ultraviolet B irradiation of the mouse eye induces pigmentation of the skin more strongly than does stress loading, by increasing the levels of prohormone convertase 2 and α-melanocyte-stimulating hormone

Background.  In previous studies, we made the unexpected finding that in mice, ultraviolet (UV)B irradiation of the eye increased the concentration of α‐melanocyte‐stimulating hormone (α‐MSH) in plasma, and systemically stimulated epidermal melanocytes.

Ultraviolet‐A Irradiation to the Eye Modulates Intestinal Mucosal Functions and Properties of Mast Cells in the Mouse

We previously reported that topical irradiation of the eye by ultraviolet‐B (UVB) activated hypothalamo‐pituitary‐adrenal axis (HPA‐A) of the mouse to increase 3, 4‐dihydroxyphenylalanine (DOPA)‐positive melanocytes in the skin by an inducible nitric oxide synthase (iNOS)‐dependent mechanism. This work demonstrates that irradiation of the eye by ultraviolet‐A (UVA) specifically increased DOPA‐positive cells in the mucosa of the jejunum and colon of C57BL/6J mice by some HPA‐ and iNOS‐independent mechanism. UVA‐induced increase in DOPA‐positive cells in the intestine was inhibited by the administration of hexamethonium or prazosin plus propranolol, blockers for the sympathetic nervous system. UVA irradiation of the eye increased DOPA‐ and histidine decarboxylase (HDC)‐positive cells in the intestinal mucosa of both C57BL/6J and WBB6F1/J mice but not in the mutant strain W/Wv of the latter that lack mast cells. UVA irradiation of the eye suppressed the intestinal peristalsis of control, hypophysectomized or iNOS−/− C57BL/6J mice by the mechanism that was inhibited by hexamethonium or prazosin plus propranolol. These observations suggest that UVA irradiation of the eye stimulated the sympathetic nervous system to increase the mucosal DOPA‐ and HDC‐positive mast cells and suppressed the peristalsis of the small intestine of the mouse.

Dynamic aspects of ascorbic acid metabolism in the circulation: analysis by ascorbate oxidase with a prolonged in vivo half-life.

Because AA (L-ascorbic acid) scavenges various types of free radicals to form MDAA (monodehydroascorbic acid) and DAA (dehydroascorbic acid), its regeneration from the oxidized metabolites is critically important for humans and other animals that lack the ability to synthesize this antioxidant. To study the dynamic aspects of AA metabolism in the circulation, a long acting AOase (ascorbate oxidase) derivative was synthesized by covalently linking PEG [poly(ethylene glycol)] to the enzyme. Fairly low concentrations of the modified enzyme (PEG-AOase) rapidly decreased AA levels in isolated fresh plasma and blood samples with a concomitant increase in their levels of MDAA and DAA. In contrast, relatively high doses of PEG-AOase were required to decrease the circulating plasma AA levels of both normal rats and ODS (osteogenic disorder Shionogi) rats that lack the ability to synthesize AA. Administration of 50 units of PEG-AOase/kg of body weight rapidly decreased AA levels in plasma and the kidney without affecting the levels in other tissues, such as the liver, brain, lung, adrenal grand and skeletal muscles. PEG-AOase slightly, but significantly, decreased glutathione (GSH) levels in the liver without affecting those in other tissues. Suppression of hepatic synthesis of GSH by administration of BSO [L-buthionin-(S,R)-sulfoximine] enhanced the PEG-AOase-induced decrease in plasma AA levels. These and other results suggest that the circulating AA is reductively regenerated from MDAA extremely rapidly and that hepatic GSH plays important roles in the regeneration of this antioxidant.

The Effects of Ultraviolet Eye Irradiation on Dextran Sodium Sulfate-Induced Ulcerative Colitis in Mice.

Ultraviolet (UV) eye irradiation denatures the cells of the intestine. This study examined the action of UVA and UVB on dextran sodium sulfate (DSS)‐induced ulcerative colitis. We produced a mouse model of ulcerative colitis by administering DSS for 5 days and irradiated the eye with UVB or UVA for each day of the DSS treatment period. DSS‐induced ulcerative colitis was deteriorated by the UVB eye irradiation. Conversely, the symptoms improved with UVA eye irradiation. The levels of adrenocorticotropic hormone (ACTH), corticotropin‐releasing hormone (CRH), urocortin 2, interleukin (IL)‐18, IL‐6 and histamine in the blood increased after the UVB eye irradiation of DSS‐treated mice (UVB/DSS‐treated mice). In contrast, the β‐endorphin level in the blood of the UVA/DSS‐treated mice increased and the levels of urocortin 2, tumor necrosis factor (TNF)‐α and histamine decreased. Furthermore, in the colon, the expression of melanocortin‐2 receptors (MC2R) increased in the UVB/DSS‐treated mice, while the expression of μ‐opioid receptors increased in the UVA/DSS‐treated mice. When an ACTH inhibitor was administered, UVB eye irradiation caused the deterioration of DSS‐treated ulcerative colitis, while the effect of UV eye irradiation disappeared with a μ‐opioid receptor antagonist. These results suggested that UV eye irradiation plays an important role in DSS‐induced ulcerative colitis.

Prevention of scattered light-induced asthenopia and fatigue by a polarized filter

Background: It has been well documented that a long‐time irradiation of the eye by a strong light elicits eyestrain and fatigue. To elucidate the mechanism for the induction of light‐induced fatigue and asthenopia, changes in the mouse were analyzed after white light‐irradiation to the eye.

UVA irradiation of the eye modulates the contact hypersensitivity of the skin and intestines by affecting mast cells in mice.

Ultraviolet A (UVA) irradiation before allergic sensitization induces immunosuppression, but the precise mechanism remained unclear. In this study, we examined the influence of UVA irradiation of the eye on contact hypersensitivity (CHS) and the role of mast cells in CHS.

Ultraviolet A eye irradiation ameliorates colon carcinoma induced by azoxymethane and dextran sodium sulfate through β‐endorphin and methionine‐enkephalin

We previously reported that ultraviolet (UV) A eye irradiation reduces the ulcerative colitis induced by dextran sodium sulfate (DSS). This study examined the effects of UVA on colon carcinoma induced by azoxymethane (AOM) and DSS.

The gender differences in the inhibitory action of UVB-induced melanocyte activation by the administration of tranexamic acid.

Tranexamic acid has an inhibitory action on ultraviolet (UV) B‐induced melanocyte activation. This study examined the sex differences in the inhibitory action of tranexamic acid on UVB‐induced melanocyte activation.