dihomo γ linolenic acid

Dihomo-γ-linolenic acid (DGLA) 是一种广泛存在于植物体内的脂肪酸，具有抗肿瘤和抗增殖作用，抑制异种移植肿瘤细胞生长，可用于研究类风湿性关节炎、动脉粥样硬化和特应性皮炎等与炎症相关的疾病。

Dihomo-γ-Linolenic acid methyl ester 是 Dihomo-γ-Linolenic acid 的甲酯形式，Dihomo-γ-Linolenic acid 具有抗炎和抗增殖作用。

Ethyl dihomo-γ-linolenic acid ethyl ester (ethyl DGLA), an ω-6 fatty acid intermediate ester form, elevates prostaglandin E1(PGE1) and PGE2 secretion in rabbit renal papilla when administered dietarily at a dosage of 1 g kg per day for 25 days. Additionally, this dosage of ethyl DGLA increases triglyceride levels and enhances the proportion of 20:3ω6 and 20:4ω6 phospholipids in the renal medulla of rabbits. Ethyl DGLA formulations have been employed in managing eczema and inflammatory disorders.

Dihomo-γ-linolenic acid sodium (DGLA; all-cis-8,11,14-Eicosatrienoic acid) 是一种具有抗炎和抗增殖活性的 20 碳 ω-6 脂肪酸。Dihomo-γ-linolenic acid (sodium) 能减轻载脂蛋白 E 缺陷小鼠模型的动脉粥样硬化。

12(S)-HETrE是一种内源性代谢物，由血小板中的12-脂氧合酶（12-LOX）氧化ω-6 PUFA dihomo-γ-linolenic acid(DGLA)产生，作用于Gαs偶联的G蛋白偶联受体，具有抗血栓形成的作用，在心血管疾病具有潜在的治疗作用。12(S)-HETrE 在体外可抑制激动剂介导的血小板活化（IC50 = 40 μM）、α 颗粒分泌、整合素 αⅡbβ3 活化、Rap1 活化和凝血酶诱导的血块回缩。

8(S)-HETrE is a monohydroxy polyunsaturated fatty acid produced by rabbit neutrophil lipoxygenase when dihomo-γ-linolenic acid is used as a substrate. Although the biological activities of 8(S)-HETrE have not been well characterized, it is expected to behave similarly to 8(S)-HETE .

8,11,14-Eicosatrienoic acid, also known as dihomo-γ-linolenic acid , is a polyunsaturated fatty acid (PUFA) produced from γ-linolenic acid by the action of fatty acid elongases. It can be metabolized by the cyclooxygenase pathway to produce 1-series prostaglandins (PGs) (e.g., PGE1). (±)14(15)-EpEDE is an EpEDE acid formed from 8,11,14-eicosatrienoic acid. This monoepoxide can be generated from the PUFA, in vitro, by the action of a strong oxidizing agent. Alternatively, this compound may be produced, in vivo, by epoxidation of the PUFA by cytochrome P450 epoxygenases. The biological properties of this compound are poorly understood.

Prostaglandin D1 (PGD1) is the theoretical D-series metabolite of dihomo-γ-linolenic acid (DGLA), but to date it has not been isolated as a natural product. It is an inhibitor of ADP-induced platelet aggregation in humans with an IC50 value of 320 ng/ml, about 1/10 as potent as PGD2. 13,14-dihydro-15-keto Prostaglandin D1 (13,14-dihydro-15-keto PGD1) is the theoretical metabolite of PGD1 via the 15-hydroxy PG dehydrogenase metabolic pathway. No biological studies for this compound have been reported.

15(S)-HETrE is the hydroxy-trienoic acid resulting from 15-lipoxygenation of dihomo-γ-linolenic acid . It is an inhibitor of 5-LO in human PMNL with an IC50 value of 4.6 μM. In RBL cells, 15(S)-HETrE inhibits 5-LO, but is about 1 20 as potent as 15(S)-HpETE.

Prostaglandin F1α (PGF1α) is the putative metabolite of dihomo-γ-linolenic acid (DGLA) via the cyclooxygenase (COX) pathway. Both PGF1α and PGF2α have been shown to act as priming pheromones for male Atlantic salmon with a threshold concentration of 10-11 M. [1] PGF1α binds to the ovine corpus luteum FP receptor at only 8% of the relative potency of PGF2α. [2] It is only half as active as PGF2α in inducing human respiratory smooth muscle contractions in vitro. [3]

Prostaglandin E1 (PGE1), synthesized through cyclooxygenase-mediated metabolism of dihomo-γ-linolenic acid (DGLA), functions by inhibiting platelet aggregation (IC50= 40 nM) and enhancing vasodilation. Its analog, 13,14-dihydro-16,16-difluoro PGE1, and the metabolite, 13,14-dihydro PGE1, both retain similar anti-aggregatory properties to the original compound. The inclusion of two electron-withdrawing fluorine atoms in 13,14-dihydro-16,16-difluoro PGE1 is believed to increase molecular stability and potentially extend bioavailability by resisting hydrolytic degradation.