cis-Urocanic acid
(Synonyms: 顺式-尿刊酸; (Z)-Urocanic acid; cis-UCA) 目录号 : GC38753
cis-Urocanic acid 是一种 5-HT2A 受体激动剂。cis-Urocanic acid 以较高亲和力与 5-HT 受体结合，Kd 为 4.6 nM。cis-Urocanic acid 是一种免疫调节剂，通过与 5-HT2A 受体结合而诱导免疫抑制。
Cas No.:7699-35-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
cis-Urocanic acid is a 5-HT2A receptor agonist. cis-Urocanic acid binds to 5-HT receptor with relatively high affinity (Kd=4.6 nM). cis-Urocanic acid is an immune modulator that induces immunosuppression by binding to the 5-HT2A receptor[1].
Treatment with 100 μg/mL cis-Urocanic acid (cis-UCA) completely suppresses IL-6 and IL-8 secretion, decreases caspase-3 activity, and improves cell viability against UV-B irradiation. No significant effects on IL-6 or IL-8 secretion, caspase-3 activity, or viability of the non-irradiated cells are observed with 100 μg/mL cis-Urocanic acid in both cell types. The 5000 μg/mL concentration is toxic[1]. Cell Viability Assay[1] Cell Line: Human corneal epithelial cells (HCE-2) and human conjunctival epithelial cells (HCECs)
[1]. Walterscheid JP, et al. Cis-urocanic acid, a sunlight-induced immunosuppressive factor, activates immune suppression via the 5-HT2A receptor. Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17420-5. [2]. Viiri J, et al. Cis-urocanic acid suppresses UV-B-induced interleukin-6 and -8 secretion and cytotoxicity in human corneal and conjunctival epithelial cells in vitro. Mol Vis. 2009 Sep 8;15:1799-805.
| Cas No. | 7699-35-6 | SDF | |
| 别名 | 顺式-尿刊酸; (Z)-Urocanic acid; cis-UCA | ||
| Canonical SMILES | O=C(O)/C=C\C1=CN=CN1 | ||
| 分子式 | C6H6N2O2 | 分子量 | 138.12 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 7.2401 mL | 36.2004 mL | 72.4008 mL |
| 5 mM | 1.448 mL | 7.2401 mL | 14.4802 mL |
| 10 mM | 0.724 mL | 3.62 mL | 7.2401 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
cis-Urocanic acid as a mediator of ultraviolet-light-induced immunosuppression
Semin Hematol 1992 Apr;29(2):102-7.PMID:1594941doi
Treatment of an organism with UVB light or PUVA (8-methoxypsoralen + UVA light) not only leads to alterations in the irradiated skin but also to systemic immunomodulation, due to the release of several chemical mediators of immunosuppression like prostaglandins, acute-phase proteins, IL-1 inhibitor, alpha-melanocyte-stimulating hormone, propiomelanocorticotropin or other cytokines. A recently described mediator is urocanic acid, which is transformed by UV light in the skin from the trans- to the cis-isomer and that exerts a systemic immunomodulatory effect. In our experiments, treatment with PUVA or with cis-Urocanic acid prevents the rejection of rat heart allografts in 50% and 40% of cases, respectively. Control grafts are rejected in fewer than 10 days. PUVA treatment of donor leukocytes before transfusion into the prospective recipient inhibits only their sensitizing, not their graft-protecting, effect on subsequent skin grafts in mice. PUVA treatment also prevents acute lethal GVH disease in mice after irradiation with a sublethal dose of x-rays and transfusion of semiallogeneic spleen cells. Treatment of recipient mice with cis-Urocanic acid has the same effect. The humoral immune response to sheep erythrocytes is not influenced by cis-Urocanic acid. These results demonstrate that PUVA treatment or its chemical mediator, cis-Urocanic acid, may be used in transplantation and hematology as naturally occurring immunosuppressive agents, especially for the control and manipulation of GVH leukemia reaction.
Studies to determine the immunomodulating effects of cis-Urocanic acid
Methods 2002 Sep;28(1):63-70.PMID:12231189DOI:10.1016/s1046-2023(02)00210-4.
Exposure to ultraviolet (UV) radiation, particularly the UVB wavelengths, leads not only to DNA damage but also to suppression of cell-mediated immunity to antigens encountered shortly after the irradiation. One initiator of this complex process is cis-Urocanic acid (cis-UCA), which is formed from the naturally occurring trans isomer in the epidermis on absorption of UV. cis-UCA has been shown to have immunomodulating properties in a variety of in vivo and in vitro experimental systems, although its mechanism of action is not yet clear. This article covers methods of preparing cis-UCA and of analyzing UCA isomers in various human and mouse tissues. Experiments that demonstrate that cis-UCA is immunosuppressive are described. The final section deals with the preparation and characterization of a monoclonal antibody with specificity for cis-UCA.
cis-Urocanic acid stimulates neuropeptide release from peripheral sensory nerves
J Invest Dermatol 2001 Oct;117(4):886-91.PMID:11676828DOI:10.1046/j.0022-202x.2001.01466.x.
Previous studies using an antibody to cis-Urocanic acid and mast-cell-depleted mice implicated both cis-Urocanic acid and mast cells in the mechanisms by which ultraviolet B light suppresses systemic contact hypersensitivity responses in mice. In the absence of a direct stimulatory effect of cis-Urocanic acid on connective tissue mast cells, an indirect association was investigated. A blister induced in the rat hind footpad was used to examine the effects of slowly perfused cis-Urocanic acid on cutaneous blood flow. cis-Urocanic acid but not trans-urocanic acid increased microvascular flow by a mechanism largely dependent on the combined activity of the neuropeptides, substance P and calcitonin gene-related peptide. Perfusion of cis-Urocanic acid over the base of blisters induced in sensory-neuropeptide-depleted rats did not have any stimulatory effect above that seen with perfusion of cis-Urocanic acid together with neuropeptide receptor antagonists in control rats. There was a small direct effect of cis-Urocanic acid on microvascular blood flow. As both substance P and calcitonin gene-related peptide could directly degranulate connective tissue mast cells, this study suggests that cis-Urocanic acid indirectly activates mast cells via its effects on peripheral terminals of unmyelinated primary afferent sensory nerves. cis-Urocanic-acid-induced neuropeptides may also contribute to ultraviolet-B-induced cutaneous inflammation and alterations to Langerhans cell activity.
Urocanic acid and immunosuppression
Photochem Photobiol 1989 Aug;50(2):267-75.PMID:2675139DOI:10.1111/j.1751-1097.1989.tb04159.x.
Urocanic acid, a molecule found at high concentration in the stratum corneum, acts as a photoreceptor for UV-light, isomerizing from the naturally occurring trans-form to the cis-form. It has been proposed that cis-Urocanic acid may mediate the transient alteration in immune surveillance resulting in immunosuppression induced after UV-irradiation, by interacting with immune cells locally and/or systemically to generate T cells with suppressor function. The evidence to support this hypothesis is summarized, and possible interactions of urocanic acid with immune cells and their outcome are discussed.
cis-Urocanic acid attenuates acute dextran sodium sulphate-induced intestinal inflammation
PLoS One 2010 Oct 27;5(10):e13676.PMID:21060867DOI:10.1371/journal.pone.0013676.
On exposure to sunlight, urocanic acid (UCA) in the skin is converted from trans to the cis form and distributed systemically where it confers systemic immunosuppression. The aim of this study was to determine if administration of cis-UCA would be effective in attenuating colitis and the possible role of IL-10. Colitis was induced in 129/SvEv mice by administering 5% dextran sodium sulfate (DSS) for 7 days in drinking water. During this period mice received daily subcutaneously injections of cis-UCA or vehicle. To examine a role for IL-10, 129/SvEv IL-10(-/-) mice were injected for 24 days with cis-UCA or vehicle. Clinical disease was assessed by measurement of body weight, stool consistency, and presence of blood. At sacrifice, colonic tissue was collected for histology and measurement of myeloperoxidase and cytokines. Splenocytes were analyzed for CD4+CD25+FoxP3+ T-regulatory cells via flow cytometry. Murine bone-marrow derived antigen-presenting cells were treated with lipopolysaccharide (LPS) ± UCA and cytokine secretion measured. Our results demonstrated that cis-UCA at a dose of 50 µg was effective in ameliorating DSS-induced colitis as evidenced by reduced weight loss and attenuated changes in colon weight/length. This protection was associated with reduced colonic expression of CXCL1, an increased expression of IL-17A and a significant preservation of splenic CD4+CD25+FoxP3+ T-regulatory cells. cis-UCA decreased LPS induced CXCL1, but not TNFα secretion, from antigen-presenting cells in vitro. UCA reduced colonic levels of IFNγ in IL-10(-/-) mice but did not attenuate colitis. In conclusion, this study demonstrates that cis-Urocanic acid is effective in reducing the severity of colitis in a chemically-induced mouse model, indicating that pathways induced by ultraviolet radiation to the skin can influence distal sites of inflammation. This provides further evidence for a possible role for sunlight exposure in modulating inflammatory disorders.