更新于：2024-11-01

Platelet-activating factor x Arachidonic acid

更新于：2024-11-01

基本信息

关联

项与 Platelet-activating factor x Arachidonic acid 相关的药物

AGN-191743

靶点

Arachidonic acid x Platelet-activating factor

作用机制

花生四烯酸抑制剂 [+2]

在研机构-

原研机构

F. Hoffmann-La Roche Ltd.

在研适应症-

非在研适应症

特应性皮炎 [+1]

最高研发阶段终止

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 Platelet-activating factor x Arachidonic acid 相关的临床结果

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100 项与 Platelet-activating factor x Arachidonic acid 相关的转化医学

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0 项与 Platelet-activating factor x Arachidonic acid 相关的专利（医药）

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项与 Platelet-activating factor x Arachidonic acid 相关的文献（医药）

2013-01-01·North American Journal of Medical Sciences

Anaphylactic shock: Kounis hypersensitivity-associated syndrome seems to be the primary cause

Review

作者: Hahalis, George ; Kounis, Nicholas G ; Soufras, George D

Experiments have shown that anaphylaxis decreases cardiac output; increases left ventricular end diastolic pressure; induces severe early acute increase in respiratory resistance with pulmonary interstitial edema; and decreases splanchnic, cerebral, and myocardial blood flow more than what would be expected from severe arterial dilation and hypotension. This is attributed to the constrictive action of inflammatory mediators released during anaphylactic shock. Inflammatory mediators such as histamine, neutral proteases, arachidonic acid products, platelet-activating factor (PAF), and a variety of cytokines and chemokines constitute the pathophysiologic basis of Kounis hypersensitivity-associated acute coronary syndrome. Although the mechanisms of anaphylactic shock still remain to be elucidated, myocardial involvement due to vasospasm-induced coronary blood flow reduction manifesting as Kounis syndrome should be always considered. Searching current experimental and clinical literature on anaphylactic shock pathophysiology, causality, clinical appearance, and treatment via PubMed showed that differentiating global hypoperfusion from primary tissue suppression due to mast cell mediator constrictive action on systemic arterial vasculature is a challenging procedure. Combined tissue suppression from arterial involvement and peripheral vasodilatation, perhaps, occur simultaneously. In cases of anaphylactic shock treatment targeting the primary cause of anaphylaxis together with protection of coronary vasculature and subsequently the cardiac tissue seems to be of paramount importance.

2008-05-01·Journal of Urology1区 · 医学

The Arachidonic Acid Pathway and its Role in Prostate Cancer Development and Progression

1区 · 医学

Review

作者: Dong, Qihan ; Kurek, Caroline ; Patel, Manish I.

PURPOSEThe arachidonic acid pathway incorporates phospholipase, cyclooxygenase, lipoxygenase and epoxygenase enzymes. This pathway has been shown to have a major role in the development and progression of a number of cancers, including prostate cancer. We discuss the current status of research of this pathway in the area of prostate cancer, ranging from preclinical in vitro studies to human clinical trials.MATERIALS AND METHODSWe performed an online search of the current and past peer reviewed literature on prostate cancer and arachidonic acid, phospholipase, cyclooxygenase, lipoxygenase, epoxygenase, platelet activating factor, prostaglandin and eicosanoid. We retrieved and evaluated all full-length articles published in English from the 1980s to January 2007.RESULTSEpidemiological evidence suggested that nonsteroidal anti-inflammatory drugs may decrease the risk of prostate cancer. This effect, presumably through the inhibition of cyclooxygenase-2, has been validated in preclinical studies. Cyclooxygenase-2 inhibition has also decreased the rate of prostate specific antigen increase in men with biochemical recurrence after treatment for prostate cancer. Although lipoxygenase and secretory phospholipase A2 inhibition was also effective for decreasing prostate cancer growth in preclinical studies, to our knowledge these strategies have not yet been used in clinical trials. Cytosolic phospholipase A2, platelet activating factor and epoxygenase need further investigation to determine a role in prostate cancer.CONCLUSIONSEvolving data suggest a significant role for some areas of the arachidonic acid pathway in prostate cancer. Inhibiting 1 or a number of these enzymes in combination may hold promise for future prostate cancer treatment.

1989-11-01·Clinical Immunology and Immunopathology

New concepts in the pathogenesis of asthma

Review

作者: Larsen, G L

Heightened airways reactivity is a major characteristic of asthma. Several stimuli capable of producing an inflammatory reaction within the respiratory tract can increase airways reactivity in both normal and asthmatic subjects. The association between lower airways inflammation and alterations in airways function has been studied most extensively after antigen exposure leading to an immediate and/or late asthmatic response in atopic subjects. The late asthmatic response (LAR) is of special interest because it lasts for hours, is prevented by corticosteroids and not adrenergic agents, and is associated with more severe asthma as well as increases in airways responsiveness. While late phase reactions in the lung and skin were initially thought to be Arthus reactions, more recent observations in man and animal models suggest they may be initiated when antigen-specific IgE is present, and may be blunted by antigen-specific IgG. In terms of pathology, immediate reactions are characterized primarily by edema while late phase reactions are associated with infiltration of the involved tissues with inflammatory cells. The potential importance of granulocytes to the reactions in the skin of rats and the lungs of rabbits was suggested when cytotoxic drugs that produced granulocytopenia prevented late phase responses. Several other factors also appear to be important in determining if an LAR will occur. These include the antigen load, level of airways reactivity, histamine releasing factors, lymphocyte populations within the lung, and endogenous corticosteroid levels. While various mediators of inflammation and hypersensitivity such as platelet activating factor and cyclooxygenase and lipoxygenase products of arachidonic acid metabolism produce some of the clinical features seen in asthma, one mediator is unlikely to be responsible for all the manifestations of this disorder. Rather, a series of cell-to-cell interactions mediated through the products they release are likely to produce the pathologic and physiologic features of the disease.