Recent Progress in Prostaglandin F2αEthanolamide (Prostamide F2α) Research and Therapeutics

Woodward, David F.; Wang, J. W.; Poloso, Neil J.

doi:10.1124/pr.112.007088

Cited by 45 publications

(28 citation statements)

References 84 publications

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“…Появление таких лекарств позволило бы реализовать совершенно новую концепцию ле-чения многих заболеваний, основанную не на подавлении тех или иных проявлений патологического процесса, а на стиму-ляции естественного разрешения воспалительной реакции и репарации ткани. К счастью, создание таких препаратов яв-ляется вполне доступной задачей, поскольку фармакологи имеют серьезный опыт производства устойчивых и активных аналогов других эйкозаноидов, в частности ПГЕ1 (алпроста-дил и мизопростол), ПГF2α (биматопрост и динопрост) и про-стациклина (илопрост) [113][114][115][116]. Так, «первая ласточка» здесь уже появилась: это RX-10045, стабильный аналог РВЕ1.…”

Section: фармакологическое воздействие на метаболизм эйкозаноидов: прunclassified

Eicosanoids and Inflammation

Каратеев¹,

Алейникова²

2016

RJTAO

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Главный принцип современной терапии -целенапра-вленный патогенетический подход, в соответствии с кото-рым основной целью лекарственного или немедикамен-тозного воздействия становятся ключевые элементы раз-вития болезни.Одной из наиболее перспективных «мишеней» фар-макотерапии представляется воспаление. Это связано с тем, что воспалительный процесс лежит в основе патоге-неза практически всех болезней и патологических состо-яний [1, 2]. Очевидно, что локальное и системное воспа-ление определяет развитие «воспалительной» патологии, связанной с инфекционной или аутоиммунной агресси-ей, оно сопровождает любые травмы и ранения, играет принципиальную роль в прогрессировании злокачествен-ных новообразований [3][4][5]. Не вызывает сомнения и важнейшее значение воспалительной реакции в развитии таких болезней, как остеоартрит (ОА), атеросклероз и нейродегенеративные заболевания, которые ранее рас-сматривались как «дегенеративные» или «обменные» [6][7][8].

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Section: фармакологическое воздействие на метаболизм эйкозаноидов: прunclassified

Eicosanoids and Inflammation

Каратеев¹,

Алейникова²

2016

RJTAO

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“…Therefore, eCB-derived PGs form a bioactive signaling network discrete from AA-derived PGs. Efforts to categorize the effects of eCB-derived PG-EAs and PG-Gs are accelerating in part due to the availability of novel pharmacological tools including PGF 2α -EA receptor agonists and antagonists (for review see [55]) as well as COX-2 inhibitors that differentially inhibit PG-EA and PG-G production by COX-2 without affecting AA-derived PGs.…”

Section: Oxygenation Of Endocannabinoids By Cox-2mentioning

confidence: 99%

Substrate-selective COX-2 inhibition as a novel strategy for therapeutic endocannabinoid augmentation

Hermanson

Gamble-George

Marnett

et al. 2014

Trends in Pharmacological Sciences

103

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Pharmacologic augmentation of endogenous cannabinoid (eCB) signaling is an emerging therapeutic approach for the treatment of a broad range of pathophysiological conditions. Thus far, pharmacological approaches have focused on inhibition of canonical eCB inactivation pathways, fatty acid amide hydrolase for anandamide and monoacylglycerol lipase for 2-arachidonoylglycerol. Here we review experimental evidence that cyclooxygenase-2-mediated eCB oxygenation represents a third mechanism for terminating eCB action at cannabinoid receptors. We describe the development, molecular mechanisms, and in vivo validation of “substrate-selective” COX-2 inhibitors that prevent eCB inactivation by COX-2 without affecting the prostaglandin generation from arachidonic acid. Lastly, we review recent data on the potential therapeutic applications of substrate-selective COX-2 inhibitors with a focus on neuropsychiatric disorders.

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“…Interestingly, several recent studies demonstrated that COX-2 can convert 2-AG to prostaglandin-glyceryl esters, whereas it can convert AEA to prostaglandin-ethanolamides (prostamides) (231). Among these endocannabinoid metabolites, prostaglandin F 2␣ ethanolamide (prostamide F 2␣ ) is the most intensively studied species with marked effects on intraocular pressure, hair growth, fat deposition, and nociception (253).…”

Section: Cerebrovascular Actions Of Exogenous and Endogenous Cannabinmentioning

confidence: 99%

Endocannabinoids in cerebrovascular regulation

Benyó

Ruisanchez

Leszl-Ishiguro

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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The cerebral blood flow is tightly regulated by myogenic, endothelial, metabolic, and neural mechanisms under physiological conditions, and a large body of recent evidence indicates that inflammatory pathways have a major influence on the cerebral blood perfusion in certain central nervous system disorders, like hemorrhagic and ischemic stroke, traumatic brain injury, and vascular dementia. All major cell types involved in cerebrovascular control pathways (i.e., smooth muscle, endothelium, neurons, astrocytes, pericytes, microglia, and leukocytes) are capable of synthesizing endocannabinoids and/or express some or several of their target proteins [i.e., the cannabinoid 1 and 2 (CB1 and CB2) receptors and the transient receptor potential vanilloid type 1 ion channel]. Therefore, the endocannabinoid system may importantly modulate the regulation of cerebral circulation under physiological and pathophysiological conditions in a very complex manner. Experimental data accumulated since the late 1990s indicate that the direct effect of cannabinoids on cerebral vessels is vasodilation mediated, at least in part, by CB1 receptors. Cannabinoid-induced cerebrovascular relaxation involves both a direct inhibition of smooth muscle contractility and a release of vasodilator mediator(s) from the endothelium. However, under stress conditions (e.g., in conscious restrained animals or during hypoxia and hypercapnia), cannabinoid receptor activation was shown to induce a reduction of the cerebral blood flow, probably via inhibition of the electrical and/or metabolic activity of neurons. Finally, in certain cerebrovascular pathologies (e.g., subarachnoid hemorrhage, as well as traumatic and ischemic brain injury), activation of CB2 (and probably yet unidentified non-CB1/non-CB2) receptors appear to improve the blood perfusion of the brain via attenuating vascular inflammation. cerebral circulation; endocannabinoids; cannabinoid receptors; TRPV1 channel; neurovascular unit THE CEREBRAL VASCULATURE HAS two main homeostatic functions: 1) to adjust the local blood supply to the eventually rapidly changing metabolic demands of neurons; and 2) to maintain an optimal extracellular environment in the brain. The former function is realized by the regulation of the local cerebral blood flow (CBF), whereas the latter is achieved by the maintenance of the blood-brain barrier (BBB) and related transport mechanisms. The endocannabinoid system has been implicated as an important regulatory component in both of these cerebrovascular functions. The roles of endocannabinoids and cannabinoid receptors in the BBB have been reviewed recently (237). Here we aim to overview our knowledge on the endocannabinoid-mediated regulation of cerebral circulation.

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Recent Progress in Prostaglandin F₂_αEthanolamide (Prostamide F₂_α) Research and Therapeutics

Cited by 45 publications

References 84 publications

Eicosanoids and Inflammation

Eicosanoids and Inflammation

Substrate-selective COX-2 inhibition as a novel strategy for therapeutic endocannabinoid augmentation

Endocannabinoids in cerebrovascular regulation

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