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auda 12  (MedChemExpress)


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    MedChemExpress auda 12
    Auda 12, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 92 stars, based on 5 article reviews
    auda 12 - by Bioz Stars, 2026-03
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    Effect of eicosanoid inhibitors on Plasmodium oocyst survival. Biosynthesis pathways of eicosanoids as described in mammalian systems are summarized in ( A ). Arachidonic acid (AA) is derived from membrane phospholipids by hydrolysis of phospholipase A2 (PLA2) activity. The AA is further metabolized into various eicosanoids, such as prostaglandins (PGs), leukotrienes (LTs), lipoxins (LXs) and dihydroxyeicosatrienoic acids (DHETs) through the activity of specific enzymes, cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP), and epoxide hydrolase (EH), respectively. The influence of specific eicosanoid inhibitors on P. berghei survival was addressed in mosquitoes injected with each respective inhibitor by examining oocyst numbers at 8 days post-infection ( B – E ). Compared to an ethanol (EtOH) control, oocyst survival was examined for the PLA2 inhibitor, dexamethasone (DEX) ( B ), a COX inhibitor, indomethacin (INDO) ( C ), a LOX inhibitor, esculetin (ES) ( D ), and an epoxide hydrolase inhibitor, AUDA ( E ). Data were analyzed by Mann-Whitney U using GraphPad Prism 6.0. Bar graphs represent mean ± SEM of three independent experiments. Asterisks denote significance (* p < 0.05); ns, not significant.

    Journal: Insects

    Article Title: Inhibitors of Eicosanoid Biosynthesis Reveal that Multiple Lipid Signaling Pathways Influence Malaria Parasite Survival in Anopheles gambiae

    doi: 10.3390/insects10100307

    Figure Lengend Snippet: Effect of eicosanoid inhibitors on Plasmodium oocyst survival. Biosynthesis pathways of eicosanoids as described in mammalian systems are summarized in ( A ). Arachidonic acid (AA) is derived from membrane phospholipids by hydrolysis of phospholipase A2 (PLA2) activity. The AA is further metabolized into various eicosanoids, such as prostaglandins (PGs), leukotrienes (LTs), lipoxins (LXs) and dihydroxyeicosatrienoic acids (DHETs) through the activity of specific enzymes, cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP), and epoxide hydrolase (EH), respectively. The influence of specific eicosanoid inhibitors on P. berghei survival was addressed in mosquitoes injected with each respective inhibitor by examining oocyst numbers at 8 days post-infection ( B – E ). Compared to an ethanol (EtOH) control, oocyst survival was examined for the PLA2 inhibitor, dexamethasone (DEX) ( B ), a COX inhibitor, indomethacin (INDO) ( C ), a LOX inhibitor, esculetin (ES) ( D ), and an epoxide hydrolase inhibitor, AUDA ( E ). Data were analyzed by Mann-Whitney U using GraphPad Prism 6.0. Bar graphs represent mean ± SEM of three independent experiments. Asterisks denote significance (* p < 0.05); ns, not significant.

    Article Snippet: Dexamethasone ((11β,16α)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione) a phospholipase A2 inhibitor, indomethacin (1-(4-Chlorobenzoyl)-5-methoxy-2-methyl-3-indoleacetic acid) a cyclooxygenase (COX) inhibitor, esculetin (6,7-Dihydroxycoumarin) a lipoxygenase (LOX) inhibitor, and AUDA (12-[[(tricyclo[3.3.1.13,7] dec-1-ylamino) carbonyl]amino]-dodecanoic acid) an epoxide hydrolase inhibitor, were purchased from Sigma-Aldrich.

    Techniques: Derivative Assay, Activity Assay, Injection, Infection, MANN-WHITNEY