Pristane
(Synonyms: 姥鲛烷, Norphytane) 目录号 : GC64748
Pristane (2,6,10,14-Tetramethylpentadecane, TMPD) is a natural saturated terpenoid alkane obtained primarily from shark liver oil that is widely used to induce tumorgenesis in mice and arthritis and lupus nephritis in rats.
Cas No.:1921-70-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Pristane (2,6,10,14-Tetramethylpentadecane, TMPD) is a natural saturated terpenoid alkane obtained primarily from shark liver oil that is widely used to induce tumorgenesis in mice and arthritis and lupus nephritis in rats.
[1] M Satoh, et al. Clin Exp Immunol . 2000 Aug;121(2):399-405. [2] K Gadó, et al. Haematologica . 2001 Mar;86(3):227-36. [3] R Holmdahl, et al. Immunol Rev . 2001 Dec;184:184-202.
| Cas No. | 1921-70-6 | SDF | Download SDF |
| 别名 | 姥鲛烷, Norphytane | ||
| 分子式 | C19H40 | 分子量 | 268.52 |
| 溶解度 | DMSO : 100 mg/mL (372.41 mM; Need ultrasonic) | 储存条件 | Store at -20°C, protect from light |
| 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 | 3.7241 mL | 18.6206 mL | 37.2412 mL |
| 5 mM | 0.7448 mL | 3.7241 mL | 7.4482 mL |
| 10 mM | 0.3724 mL | 1.8621 mL | 3.7241 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。
Pristane-induced mammary carcinomas
Methods Cell Biol 2021;163:187-195.PMID:33785165DOI:10.1016/bs.mcb.2020.10.016.
Animal models for studying human breast cancer carcinogenesis and testing drug candidates on human breast cancer have extensively been proposed. Especially, chemically induced breast tumor models have been used because they can mimic the progression of clinical cancer from the beginning and can be generated with a facile procedure. Pristane is a hydrocarbon oil that is used as a chemical carcinogen to induce tumorigenesis in mice as well as arthritis and lupus nephritis in rats. In only a few studies, pristane-induced breast cancer models have been reported. This chapter is designated to describe pristane-induced mammary carcinoma models. Here, we provide a protocol for generating pristane-induced breast tumors in mice models for analyzing and for testing potential therapeutics on them. The given protocol can be applied to other animal models with some changes.
Oxidative DNA Damage Accelerates Skin Inflammation in Pristane-Induced Lupus Model
Front Immunol 2020 Sep 24;11:554725.PMID:33072095DOI:10.3389/fimmu.2020.554725.
Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease in which type I interferons (IFN) play a key role. The IFN response can be triggered when oxidized DNA engages the cytosolic DNA sensing platform cGAS-STING, but the repair mechanisms that modulate this process and govern disease progression are unclear. To gain insight into this biology, we interrogated the role of oxyguanine glycosylase 1 (OGG1), which repairs oxidized guanine 8-Oxo-2'-deoxyguanosine (8-OH-dG), in the pristane-induced mouse model of SLE. Ogg1-/- mice showed increased influx of Ly6Chi monocytes into the peritoneal cavity and enhanced IFN-driven gene expression in response to short-term exposure to Pristane. Loss of Ogg1 was associated with increased auto-antibodies (anti-dsDNA and anti-RNP), higher total IgG, and expression of interferon stimulated genes (ISG) to longer exposure to Pristane, accompanied by aggravated skin pathology such as hair loss, thicker epidermis, and increased deposition of IgG in skin lesions. Supporting a role for type I IFNs in this model, skin lesions of Ogg1-/- mice had significantly higher expression of type I IFN genes (Isg15, Irf9, and Ifnb). In keeping with loss of Ogg1 resulting in dysregulated IFN responses, enhanced basal and cGAMP-dependent Ifnb expression was observed in BMDMs from Ogg1-/- mice. Use of the STING inhibitor, H151, reduced both basal and cGAMP-driven increases, indicating that OGG1 regulates Ifnb expression through the cGAS-STING pathway. Finally, in support for a role for OGG1 in the pathology of cutaneous disease, reduced OGG1 expression in monocytes associated with skin involvement in SLE patients and the expression of OGG1 was significantly lower in lesional skin compared with non-lesional skin in patients with Discoid Lupus. Taken together, these data support an important role for OGG1 in protecting against IFN production and SLE skin disease.
Production of Pristane and phytane in the marine environment: role of prokaryotes
Res Microbiol 2011 Nov;162(9):923-33.PMID:21288485DOI:10.1016/j.resmic.2011.01.012.
This paper reviews studies dealing with the formation of Pristane and phytane in the marine environment and focuses on the role played by prokaryotes in these processes. Prokaryotes may notably: (i) contribute to the formation of Pristane during invertebrate feeding; (ii) hydrogenate isomeric pristenes and phytenes arising from degradation of the chlorophyll phytyl side-chain and/or α-tocopherol (vitamin E) to Pristane and phytane, respectively; and (iii) convert trimeric oxidation products of α-tocopherol (produced abiotically in the water column and in the oxic zone of sediments) to Pristane. Moreover, thermal maturation of isoprenoid components of archaea (isopranyl glyceryl ethers) also constitutes another potential source of Pristane and phytane in thermally mature sediments. Prokaryotes thus appear to play a key role in formation of these isoprenoid alkanes in the marine environment.
Pristane attenuates atherosclerosis in Apoe-/- mice via IL-4-secreting regulatory plasma cell-mediated M2 macrophage polarization
Biomed Pharmacother 2022 Nov;155:113750.PMID:36271544DOI:10.1016/j.biopha.2022.113750.
Atherosclerosis, an inflammatory progressive vascular disease, causes heart disease and stroke worldwide. B cells with immune suppressive functions have been implicated in autoimmune, inflammatory, and cardiovascular diseases. However, the precise role of regulatory B cells and the interaction with macrophages in atherosclerosis remains undefined. In our study, eight-week-old female apolipoprotein E null (Apoe-/-) mice were treated with a single dose of vehicle or Pristane and then placed on an atherogenic diet for 12 weeks. We found that Pristane decreased atherosclerotic lesion formation and increased stability of atherosclerotic plaques in Apoe-/- mice. We also observed lower frequencies of CD19+ B cells but higher frequencies of CD138+ plasma cells and CD206+ M2 macrophages in Apoe-/- mice treated with Pristane. Importantly, Pristane inhibited immune cell infiltration into the vascular wall. The upregulation of IL-4 in bone-marrow CD138+ plasma cells from pristane-treated Apoe-/- mice was demonstrated by RNA-sequencing (RNA-seq). Consistently, oxidized low-density lipoprotein (oxLDL) directly induced IL-4-secreting plasma cell generation in vitro. In a co-culture system incubating an anti-IL-4 neutralizing antibody, the results showed that oxLDL-induced CD138+ plasma cells could boost M2 macrophage polarization via IL-4 secretion. Our data demonstrate an unexpected role that Pristane induces IL-4-producing CD138+ regulatory plasma cell generation and M2 polarization to protect atherosclerosis development.
Induction of autoimmunity by Pristane and other naturally occurring hydrocarbons
Trends Immunol 2009 Sep;30(9):455-64.PMID:19699150DOI:10.1016/j.it.2009.06.003.
Tetramethylpentadecane (TMPD, or commonly known as Pristane)-induced lupus is a murine model of systemic lupus erythematosus (SLE). Renal disease and autoantibody production strictly depend on signaling through the interferon (IFN)-I receptor. The major source of IFN-I is immature monocytes bearing high levels of the surface marker Ly6C. Interferon production is mediated exclusively by signaling through TLR7 and the adapter protein MyD88. It is likely that endogenous TLR7 ligands such as components of small nuclear ribonucleoprotein complexes are involved in triggering disease. Lupus autoantibodies are produced in ectopic lymphoid tissue developing in response to TMPD. This model is well suited for examining links between dysregulated IFN-I production and the pathogenesis of human SLE, which like TMPD-lupus, is associated with high levels of IFN-I.