thromboxane-a2 and Pain

thromboxane-a2 has been researched along with Pain* in 5 studies

Reviews

1 review(s) available for thromboxane-a2 and Pain

ArticleYear
Anti-inflammatory drugs in the 21st century.
    Sub-cellular biochemistry, 2007, Volume: 42

    Historically, anti-inflammatory drugs had their origins in the serendipitous discovery of certain plants and their extracts being applied for the relief of pain, fever and inflammation. When salicylates were discovered in the mid-19th century to be the active components of Willow Spp., this enabled these compounds to be synthesized and from this, acetyl-salicylic acid or Aspirin was developed. Likewise, the chemical advances of the 19th-20th centuries lead to development of the non-steroidal anti-inflammatory drugs (NSAIDs), most of which were initially organic acids, but later non-acidic compounds were discovered. There were two periods of NSAID drug discovery post-World War 2, the period up to the 1970's which was the pre-prostaglandin period and thereafter up to the latter part of the last century in which their effects on prostaglandin production formed part of the screening in the drug-discovery process. Those drugs developed up to the 1980-late 90's were largely discovered empirically following screening for anti-inflammatory, analgesic and antipyretic activities in laboratory animal models. Some were successfully developed that showed low incidence of gastro-intestinal (GI) side effects (the principal adverse reaction seen with NSAIDs) than seen with their predecessors (e.g. aspirin, indomethacin, phenylbutazone); the GI reactions being detected and screened out in animal assays. In the 1990's an important discovery was made from elegant molecular and cellular biological studies that there are two cyclo-oxygenase (COX) enzyme systems controlling the production of prostanoids [prostaglandins (PGs) and thromboxane (TxA2)]; COX-1 that produces PGs and TxA2 that regulate gastrointestinal, renal, vascular and other physiological functions, and COX-2 that regulates production of PGs involved in inflammation, pain and fever. The stage was set in the 1990's for the discovery and development of drugs to selectively control COX-2 and spare the COX-1 that is central to physiological processes whose inhibition was considered a major factor in development of adverse reactions, including those in the GI tract. At the turn of this century, there was enormous commercial development following the introduction of two new highly selective COX-2 inhibitors, known as coxibs (celecoxib and rofecoxib) which were claimed to have low GI side effects. While found to have fulfilled these aims in part, an alarming turn of events took place in the late 2004 period when rofecox

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Diseases; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cytokines; Digestive System Diseases; Disease Models, Animal; Drug Delivery Systems; Drug Design; Fever; History, 19th Century; History, 20th Century; History, 21st Century; Humans; Inflammation; Isoenzymes; Neoplasms; Neurodegenerative Diseases; Pain; Prostaglandins; Signal Transduction; Stroke; Thromboxane A2

2007

Other Studies

4 other study(ies) available for thromboxane-a2 and Pain

ArticleYear
It's Not Just for Pain: A New Metabolic Function of Aspirin.
    Endocrinology, 2023, 02-11, Volume: 164, Issue:4

    Topics: Aspirin; Glucagon; Humans; Pain; Thromboxane A2

2023
Investigation of piperidine derivatives in ex vivo models of pain and platelet aggregation.
    Archives of pharmacal research, 2012, Volume: 35, Issue:11

    Piperidine derivatives are known to exhibit analgesic activities and are likely to possess the ability to block the effects of prostaglandins through inhibition of downstream signaling pathways. The present study investigated the activity of five derivatives (PD2-6) of 4-(4'-bromophenyl)-4-piperidinol (PD1), against pain and platelet aggregation mediated by the release of prostaglandins and thromboxane A2, respectively. The results showed that compound PD1 and its two phenacyl derivatives PD3 and PD5 exhibited a highly significant analgesic effect (p < 0.01), whereas PD4 and PD6 also showed significant activity. PD3, the most active analgesic compound when docked to the opioid receptor, had interactions between the oxygen of its nitro group and the amino group of ARG 573, indicating a distance of 1.2563 Å. The antiplatelet data showed that compound PD5 (4-(4'-bromo-phenyl)-4-hydroxy-1-[2-(2″,4″-dimethoxyphenyl)-2-oxo-ethyl]-piperidinium bromide) had an IC(50) = 0.06 mM, which was the most active compound, whereas PD3 was the second most active compound against platelet aggregating factor-induced aggregation with an IC(50) = 80 mM. Acetyl salicylic acid (IC(50) = 150 μM) was used as a positive control.

    Topics: Analgesics; Animals; Aspirin; Female; Humans; Inhibitory Concentration 50; Male; Mice; Pain; Piperidines; Platelet Aggregation; Platelet Aggregation Inhibitors; Prostaglandins; Receptors, Opioid; Structure-Activity Relationship; Thromboxane A2

2012
Prostaglandins: their release, biological effects and relationships to pain and inflammation.
    Cephalalgia : an international journal of headache, 1986, Volume: 6 Suppl 4

    Topics: Capillary Permeability; Dinoprostone; Epoprostenol; Humans; Inflammation; Migraine Disorders; Pain; Prostaglandins; Prostaglandins E; Thromboxane A2; Vasoconstriction; Vasodilation

1986
Peritoneal fluid prostaglandins and prostanoids in women with endometriosis, chronic pelvic inflammatory disease, and pelvic pain.
    American journal of obstetrics and gynecology, 1984, Feb-15, Volume: 148, Issue:4

    Peritoneal fluid obtained at laparoscopy from 49 women was measured for its content of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), 6-keto-prostaglandin F1 alpha (6-KF), and thromboxane B2 (TxB2) by specific radioimmunoassays. In normal women (n = 10), the concentrations of prostaglandins in peritoneal fluid were (mean +/- SE): PGE2 = 0.79 +/- 0.26, PGF2 alpha = 0.60 +/- 0.18, 6-KF = 0.48 +/- 0.19, and TxB2 = 0.23 +/- 0.09 ng/ml; in women with endometriosis (n = 16): PGE2 = 1.43 +/- 0.72, PGF2 alpha = 1.52 +/- 0.59, 6-KF = 3.32 +/- 0.71, and TxB2 = 1.14 +/- 0.69 ng/ml; in women with chronic pelvic inflammatory disease and/or obstructed tubes (n = 19): PGE2 = 1.94 +/- 1.04, PGF2 alpha = 1.20 +/- 0.61, 6-KF = 1.55 +/- 0.40, and TxB2 = 0.64 +/- 0.24 ng/ml; in women with pelvic pain without any visible pathologic condition (n = 4): PGE2 = 1.11 +/- 0.66, PGF2 alpha = 0.73 +/- 0.55, 6-KF = 1.35 +/- 0.35, and TxB2 = 0.39 +/- 0.17. The mean volumes of peritoneal fluid recovered were 10 to 16 ml and were not significantly different between the groups. Except for a significantly elevated concentration of 6-KF in the peritoneal fluid of women with endometriosis compared to normal women (p = less than 0.02), the prostaglandins measured did not differ significantly between the groups of women studied. The possible significance of elevated 6-KF in the peritoneal fluid of women with endometriosis is discussed.

    Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Ascitic Fluid; Chronic Disease; Dinoprost; Dinoprostone; Endometriosis; Epoprostenol; Female; Humans; Pain; Pelvic Inflammatory Disease; Pelvis; Prostaglandins; Prostaglandins E; Prostaglandins F; Thromboxane A2

1984