12(S)-HHTrE
(Synonyms: 12(S)-HHTrE) 目录号 : GC41883An agonist of BLT2
Cas No.:54397-84-1
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
12(S)-HHTrE is a product of the cyclooxygenase (COX) pathway and one of the primary arachidonic acid metabolites of human platelets. It is biosynthesized by thromboxane (TXA2) synthase from prostaglandin H2 (PGH2) concurrently with TXA2. 12(S)-HHTrE is a natural lipid agonist of the leukotriene B2 receptor BLT2 in vivo that induces chemotaxis of mast cells and accelerates wound closure. 12(S)-HHTrE is avidly oxidized to 12-oxoHTrE by porcine 15-hydroxy PGDH.
Cas No. | 54397-84-1 | SDF | |
别名 | 12(S)-HHTrE | ||
Canonical SMILES | CCCCC[C@H](O)/C=C/C=C/C/C=C\CCCC(O)=O | ||
分子式 | C17H28O3 | 分子量 | 280.4 |
溶解度 | 0.1 M Na2CO3: 2 mg/ml,DMF: Miscible,DMSO: Miscible,Ethanol: Miscible,PBS pH 7.2: 0.8 mg/ml | 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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1 mg | 5 mg | 10 mg |
1 mM | 3.5663 mL | 17.8317 mL | 35.6633 mL |
5 mM | 0.7133 mL | 3.5663 mL | 7.1327 mL |
10 mM | 0.3566 mL | 1.7832 mL | 3.5663 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 | |||
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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。
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Metabolomics analysis of collagen-induced arthritis in rats and interventional effects of oral tolerance
Anal Biochem 2014 Aug 1;458:49-57.PMID:24814225DOI:10.1016/j.ab.2014.04.035.
A serum metabolomics method based on rapid resolution liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (RRLC-Q-TOF-MS) was performed for a holistic evaluation of the metabolic changes of collagen-induced arthritis (CIA) in rats and to assess the interventional effects of type II collagen (CII) in this model. Partial least-squares-discriminant analysis (PLS-DA) was employed to study the metabolic profiling of CIA rats and control rats. Ten metabolites, namely, 12(S)-HHTrE, 12(S)-HEPE, PGE2, TXB2, 12(S)-HETE, LysoPE(16:0), PE(O-18:0/0:0), Lyso-PE(18:2), Lyso-PE(20:4), and Lyso-PC(22:5) were identified as differential metabolites associated with the pathogenesis of CIA. These results suggested that dysregulation of the arachidonic acid (AA) and phospholipid metabolic networks is involved in the pathomechanism of CIA. Differential metabolomics and histopathological analyses demonstrated that CII inhibits the progress of arthritis. Furthermore, the therapeutic effects of CII on CIA may involve regulation of the disordered AA and phospholipid metabolic networks. This metabolomics study provides new insights into the pathogenesis of arthritis and, furthermore, indicates the potential mechanism underlying the significantly increased prevalence of metabolic syndrome, defined as a clustering of cardiovascular disease (CVD) risk factors, in arthritis patients.
Pharmacological approach to the pro- and anti-inflammatory effects of Ranunculus sceleratus L
J Ethnopharmacol 2003 Nov;89(1):131-7.PMID:14522444DOI:10.1016/s0378-8741(03)00271-x.
Ranunculus sceleratus is a widespread species with unique toxicological and pharmacological activities. The present study seeks to assess this species' ability, both in vitro and in vivo, to modulate processes involved in inflammations. To this end, different extracts from the aerial parts of the plant were tested in several models of acute inflammation induced by tetradecanoylphorbol acetate (TPA), arachidonic acid (AA), and carrageenan, as well as in two models of delayed hypersensitivity induced by oxazolone and dinitrofluorobencene (DNFB). The extracts were also assayed in models of eicosanoid and elastase release by intact cells. When tested in vivo, all of the extracts showed anti-inflammatory or neutral effects. In vitro, non-polar extracts of this species were able to inhibit eicosanoid production, whereas polar extracts enhanced the synthesis of 5(S)-HETE, LTB(4) and 12(S)-HHTrE. The hypothesis of a "counter-irritant" mechanism of action has thus been proposed and is also discussed herein.