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12(S)-HHTrE

(Synonyms: 12(S)-HHTrE) 目录号 : GC41883

An agonist of BLT2

12(S)-HHTrE Chemical Structure

Cas No.:54397-84-1

规格 价格 库存 购买数量
25μg
¥1,696.00
现货
50μg
¥3,221.00
现货
100μg
¥6,099.00
现货
250μg
¥13,568.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

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.

Chemical Properties

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
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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
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Research Update

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.