PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12582837-0 2003 Quinacrine abolishes increases in cytoplasmic phospholipase A2 mRNA levels in the rat hippocampus after kainate-induced neuronal injury. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 46-62 15527871-6 2005 Quinacrine, a phospholipase A2 (PLA2) inhibitor, was employed to determine its protective effect on SAM-induced PD-like changes by the inhibition of lyso-PTC formation. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-30 15527871-6 2005 Quinacrine, a phospholipase A2 (PLA2) inhibitor, was employed to determine its protective effect on SAM-induced PD-like changes by the inhibition of lyso-PTC formation. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 32-36 12814911-3 2003 Exposure of the skinned EDL fibers to indomethacin (200 microM) (n = 7) and another PLA2 inhibitor quinacrine (200 microM) (n = 5) resulted in the return of large DIFRs after use-dependent rundown. Quinacrine 99-109 phospholipase A2 group IB Rattus norvegicus 84-88 16394696-8 2006 Protein kinase C and phospholipase A2 were inhibited by chelerythrine or quinacrine, respectively. Quinacrine 73-83 phospholipase A2 group IB Rattus norvegicus 21-37 15368540-9 2005 PLA2 inhibitors quinacrine and AACOCF3, and cyclooxygenase inhibitor indomethacin blocked the effect of PLAA peptide on PKC, indicating arachidonic acid and its metabolites were involved. Quinacrine 16-26 phospholipase A2 group IB Rattus norvegicus 0-4 15371093-4 2004 Treatment with mepacrine, a phospholipase A2 inhibitor, attenuated the increases in serum and lung lavage ferritin concentrations, lung inflammation, and lung leak that occur in rats subjected to hemorrhage. Quinacrine 15-24 phospholipase A2 group IB Rattus norvegicus 28-44 12582837-1 2003 The present investigation was carried out to study the possible effects of quinacrine in modulating cytoplasmic phospholipase A(2) (cPLA(2)) mRNA levels in rat hippocampus after kainate treatment. Quinacrine 75-85 phospholipase A2 group IB Rattus norvegicus 112-130 12079427-4 2002 Crude venom induced a contraction in rat tracheal preparations through phospholipase A(2) (PLA(2)) activity, as shown by the complete and partial inhibition of contraction by PLA(2) inhibitors 4-bromophenacyl bromide and quinacrine. Quinacrine 221-231 phospholipase A2 group IB Rattus norvegicus 91-97 11786377-6 2002 Mepacrine and parabromophenacyl bromide (pBpB), two PLA(2) inhibitors, decreased the hormone-stimulated AA release to 85+/-9 and 70+/-24% respectively. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 52-58 11812506-5 2002 Consistent with our earlier work, pretreatment with the PLA(2) inhibitor quinacrine (25 mg/kg) blocked the development of cocaine and amphetamine sensitization. Quinacrine 73-83 phospholipase A2 group IB Rattus norvegicus 56-62 11774821-1 2001 OBJECTIVE: To explore the influence of quinacrine, which is an inhibitor of phospholipase A2, on gut-origin bacteria/endotoxin translocation in rats with gut ischemia/reperfusion injury. Quinacrine 39-49 phospholipase A2 group IB Rattus norvegicus 76-92 11551515-6 2001 The phospholipase A(2) (PLA(2)) inhibitor, mepacrine, completely inhibited the [14C]-AA response. Quinacrine 43-52 phospholipase A2 group IB Rattus norvegicus 4-22 11551515-6 2001 The phospholipase A(2) (PLA(2)) inhibitor, mepacrine, completely inhibited the [14C]-AA response. Quinacrine 43-52 phospholipase A2 group IB Rattus norvegicus 24-30 11278180-7 2001 The phospholipase A2 inhibitors quinacrine and p-bromophenacyl bromide added at 0.1 mM concentration each to either slices from controls or Et-DHA treated fetal brains, decreased TBARS production. Quinacrine 32-42 phospholipase A2 group IB Rattus norvegicus 4-20 11490349-4 2001 PLA(2) inhibition (quinacrine, 10 mg/kg, intravenously) was given before shock was induced. Quinacrine 19-29 phospholipase A2 group IB Rattus norvegicus 0-6 11226716-2 2001 In this investigation an attempt was made to determine a possible protective effect of quinacrine (QNC), a PLA2 inhibitor on MPTP as well as 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rodents. Quinacrine 87-97 phospholipase A2 group IB Rattus norvegicus 107-111 11226716-2 2001 In this investigation an attempt was made to determine a possible protective effect of quinacrine (QNC), a PLA2 inhibitor on MPTP as well as 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rodents. Quinacrine 99-102 phospholipase A2 group IB Rattus norvegicus 107-111 10077051-4 1999 AMs were stimulated with PLA2 or SPL rat serum, with or without administration of the PLA2 inhibitor quinacrine. Quinacrine 101-111 phospholipase A2 group IB Rattus norvegicus 86-90 10455307-7 1999 Myricetin-induced contractions were almost abolished by the phospholipase A2 (PLA2) inhibitor, quinacrine (10 microM), the cyclo-oxygenase inhibitor, indomethacin (10 microM), the thromboxane synthase inhibitor, dazoxiben (100 microM), the putative thromboxane A2 (TXA2)/prostaglandin endoperoxide receptor antagonist, ifetroban (3 microM). Quinacrine 95-105 phospholipase A2 group IB Rattus norvegicus 78-82 10535708-5 1999 The phospholipase A2 inhibitor quinacrine considerably inhibited this TEA-sensitive current, while 4-bromophenacylbromide exerted no effect. Quinacrine 31-41 phospholipase A2 group IB Rattus norvegicus 4-20 10229494-8 1999 This increase in FAME (45%) was inhibited by mepacrine (quinacrine) (10 microM), an inhibitor of PLA2. Quinacrine 45-54 phospholipase A2 group IB Rattus norvegicus 97-101 10229494-8 1999 This increase in FAME (45%) was inhibited by mepacrine (quinacrine) (10 microM), an inhibitor of PLA2. Quinacrine 56-66 phospholipase A2 group IB Rattus norvegicus 97-101 10884509-0 2000 Mechanism of suppression of cardiac L-type Ca(2+) currents by the phospholipase A(2) inhibitor mepacrine. Quinacrine 95-104 phospholipase A2 group IB Rattus norvegicus 66-84 10884509-2 2000 Mepacrine, a phospholipase A(2) inhibitor, has been shown to protect the heart from ischemic injury. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 13-31 10884509-14 2000 While mepacrine is a phospholipase A(2) inhibitor and reduces cAMP production, its inhibitory effect on I(Ca,L) mainly results from a direct block of the channel. Quinacrine 6-15 phospholipase A2 group IB Rattus norvegicus 21-39 10077051-11 1999 This lung injury was prevented by the administration of the PLA2 inhibitor quinacrine. Quinacrine 75-85 phospholipase A2 group IB Rattus norvegicus 60-64 10080140-8 1999 The damage produced by A23187 (12.5 microM) was inhibited by preincubation of cells with the PLA2 inhibitor, quinacrine (1-100 microM). Quinacrine 109-119 phospholipase A2 group IB Rattus norvegicus 93-97 9647745-3 1998 The SRE stimulation by PA was dramatically reduced by either pre-treatment with mepacrine, an inhibitor of phospholipase A2 (PLA2), or co-transfection with antisense cytosolic phospholipase A2 (cPLA2) oligonucleotide, whereas lysophosphatidic acid (LPA)-induced SRE activation was not affected. Quinacrine 80-89 phospholipase A2 group IB Rattus norvegicus 125-129 9868740-7 1998 Phospholipase A2 inhibitors, mepacrine and 4-bromophenacyl bromide, inhibited the increase in mitochondrial permeability, but did not inhibit hepatocyte death caused by CCl4. Quinacrine 29-38 phospholipase A2 group IB Rattus norvegicus 0-16 10024011-2 1999 Experiments were performed with either mepacrine (0.2 microM) or bovine serum albumin (BSA, 0.02%) which inhibits phospholipase A2 activity or binds endogenously released arachidonic acid, respectively. Quinacrine 39-48 phospholipase A2 group IB Rattus norvegicus 114-130 9312202-10 1997 Quinacrine (a PA2 inhibitor) alone had no effect on matrix vesicle PKC, but in cultures treated for 12 hours with quinacrine and 24,25-(OH)2D3, a synergistic increase in matrix vesicle PKC was observed. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-17 9312202-11 1997 Quinacrine caused a time-dependent decrease in matrix vesicle PKC and a dose- and time-dependent increase in plasma membrane PKC when incubated directly with the membranes, supporting the hypothesis that PA2 plays a role in the nongenomic regulation of PKC by 24,25-(OH)2D3. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 204-207 9263201-4 1997 These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2. Quinacrine 122-132 phospholipase A2 group IB Rattus norvegicus 87-103 9283705-12 1997 Moreover, various PLA2 inhibitors (e.g. mepacrine and dexamethasone) prevented both the early alpha, beta-meATP-induced [3H]-AA release and/or the associated long-term morphological changes, without affecting the astrocytic elongation induced by bFGF. Quinacrine 40-49 phospholipase A2 group IB Rattus norvegicus 18-22 9234831-8 1997 The EDHF-mediated dilations initiated by ACh and histamine, as well as K(ATP) activation by cromakalim, were blocked by mepacrine, a nonselective phospholipase A2 inhibitor. Quinacrine 120-129 phospholipase A2 group IB Rattus norvegicus 146-162 9249592-2 1997 Gent (10(-5) M) induced a time-dependent mesangial planar cell surface area reduction that was significantly inhibited by the PLA2 inhibitors aristolochic acid (AA) and quinacrine, by the platelet-activating factor (PAF) blocker BN-52021 (BN), and by verapamil. Quinacrine 169-179 phospholipase A2 group IB Rattus norvegicus 126-130 9177247-4 1997 The cortical induction was reduced by MK-801, an N-methyl-D-aspartic acid-receptor antagonist, and by dexamethasone and quinacrine, phospholipase A2 (PLA2) inhibiting compounds. Quinacrine 120-130 phospholipase A2 group IB Rattus norvegicus 132-148 9177247-4 1997 The cortical induction was reduced by MK-801, an N-methyl-D-aspartic acid-receptor antagonist, and by dexamethasone and quinacrine, phospholipase A2 (PLA2) inhibiting compounds. Quinacrine 120-130 phospholipase A2 group IB Rattus norvegicus 150-154 9231737-5 1997 Pretreatment of cell cultures with the PLA2 inhibitors quinacrine and aristolochic acid resulted in a dose-dependent inhibition of melittin-stimulated PKC isozyme translocation as did the inhibitor of lipoxygenase, nordihydroguaiaretic acid, whereas the cyclooxygenase inhibitor indomethacin had no effect. Quinacrine 55-65 phospholipase A2 group IB Rattus norvegicus 39-43 9160464-4 1997 Additional pharmacologic studies showed that phospholipase A2 and nitric oxide are involved in the mechanisms that produce the mechanical and thermal hyperalgesia, respectively, N omega-nitro-L-arginine methyl ester and mepacrine are relatively selective inhibitors of nitric oxide synthase and phospholipase A2, respectively. Quinacrine 220-229 phospholipase A2 group IB Rattus norvegicus 45-61 9154867-1 1997 We hypothesized that phospholipase A2 (PLA2) metabolites contribute to the acute, neutrophil-dependent, edematous lung leak that develops after administration of interleukin-1 (IL-1) intratracheally to rats and tested this premise by using mepacrine to inhibit PLA2 activity in vivo. Quinacrine 240-249 phospholipase A2 group IB Rattus norvegicus 21-37 9154867-1 1997 We hypothesized that phospholipase A2 (PLA2) metabolites contribute to the acute, neutrophil-dependent, edematous lung leak that develops after administration of interleukin-1 (IL-1) intratracheally to rats and tested this premise by using mepacrine to inhibit PLA2 activity in vivo. Quinacrine 240-249 phospholipase A2 group IB Rattus norvegicus 39-43 9263201-4 1997 These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2. Quinacrine 122-132 phospholipase A2 group IB Rattus norvegicus 105-109 9263201-4 1997 These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2. Quinacrine 122-132 phospholipase A2 group IB Rattus norvegicus 189-193 9094163-3 1997 From enzymatic assays, PLA2 and diacylglycerol (DAG) lipase were activated by Cch and respectively inhibited by the PLA2 inhibitors, mepacrine and aristolochic acid, and by the DAG lipase inhibitor, RHC 80267. Quinacrine 133-142 phospholipase A2 group IB Rattus norvegicus 23-27 9109393-4 1997 Either transfection of a dominant negative Rac mutant, RacN17, plasmid or pretreatment of mepacrine, a potent inhibitor of PLA2, blocked H2O2-induced SRE activation dramatically. Quinacrine 90-99 phospholipase A2 group IB Rattus norvegicus 123-127 9106458-0 1997 The phospholipase A2 inhibitor, quinacrine, reduces infarct size in rats after transient middle cerebral artery occlusion. Quinacrine 32-42 phospholipase A2 group IB Rattus norvegicus 4-20 9106458-2 1997 The phospholipase A2 (PLA2) inhibitor, quinacrine (5 mg/kg) or saline (of equal volume), was administered upon reperfusion to rats that underwent 2 h of middle cerebral artery occlusion (MCAO) via the intraluminal filament method. Quinacrine 39-49 phospholipase A2 group IB Rattus norvegicus 4-20 9106458-2 1997 The phospholipase A2 (PLA2) inhibitor, quinacrine (5 mg/kg) or saline (of equal volume), was administered upon reperfusion to rats that underwent 2 h of middle cerebral artery occlusion (MCAO) via the intraluminal filament method. Quinacrine 39-49 phospholipase A2 group IB Rattus norvegicus 22-26 9247325-7 1997 Moreover, a PLA2 inhibitor quinacrine inhibited the stimulatory action of ET-1 on T production and suppressed basal and ET-1-induced PGE2 release whilst a lipoxygenase blocker NDGA did not modify T response to the peptide. Quinacrine 27-37 phospholipase A2 group IB Rattus norvegicus 12-16 9062648-1 1997 Mepacrine (quinacrine) has in a number of studies been shown to protect the heart from ischemic injury, a protection commonly claimed to be due to inhibition of phospholipase A2. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 161-177 9062648-1 1997 Mepacrine (quinacrine) has in a number of studies been shown to protect the heart from ischemic injury, a protection commonly claimed to be due to inhibition of phospholipase A2. Quinacrine 11-21 phospholipase A2 group IB Rattus norvegicus 161-177 9081684-8 1997 Quinacrine, a phospholipase A2 inhibitor, suppressed ATP-induced arachidonic acid release. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-30 9031747-6 1997 The phospholipase A2 inhibitor quinacrine (30 microM) nearly completely eliminated ACh-induced hyperpolarization. Quinacrine 31-41 phospholipase A2 group IB Rattus norvegicus 4-20 9144302-0 1997 Effect of quinacrine, a phospholipase A2 inhibitor on stress and chemically induced gastroduodenal ulcers. Quinacrine 10-20 phospholipase A2 group IB Rattus norvegicus 24-40 9144302-1 1997 Quinacrine, a phospholipase A2 inhibitor, has been studied for its ability to inhibit gastric secretion and to protect the gastric and duodenal mucosa against chemically and stress-induced ulcers. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-30 8997299-7 1996 FMLP-induced impairment was normalized by the phospholipase A2 inhibitor quinacrine, the cyclooxygenase inhibitor indomethacin, and the antagonists of the prostaglandin H2 and/or thromboxane A2 receptor, ONO-3708 and S-1452, respectively. Quinacrine 73-83 phospholipase A2 group IB Rattus norvegicus 46-62 8954136-5 1996 Quinacrine, an inhibitor of phospholipase A2 activity, prevented Ca2+ release and p-hydroxymercuribenzoic acid, an inhibitor of lysophospholipid reesterification, induced a fast release of Ca2+ from isolated mitochondria. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 28-44 8836147-6 1996 The presence of quinacrine, an antagonist of PLA2, during the membrane pretreatment inhibited their fusogenic activity, suggesting the importance of activation of PLA2. Quinacrine 16-26 phospholipase A2 group IB Rattus norvegicus 45-49 8886479-6 1996 Dopamine (10 microM)-induced inhibition of Na+,K(+)-ATPase activity in WKY rats was significantly blocked by mepacrine (10 microM), a PLA2 inhibitor, suggesting the involvement of PLA2 in dopamine-mediated inhibition of Na+,K(+)-ATPase. Quinacrine 109-118 phospholipase A2 group IB Rattus norvegicus 134-138 8886479-6 1996 Dopamine (10 microM)-induced inhibition of Na+,K(+)-ATPase activity in WKY rats was significantly blocked by mepacrine (10 microM), a PLA2 inhibitor, suggesting the involvement of PLA2 in dopamine-mediated inhibition of Na+,K(+)-ATPase. Quinacrine 109-118 phospholipase A2 group IB Rattus norvegicus 180-184 9001889-1 1996 The phospholipase A2 inhibitors mepacrine, ONO-RS-082, and AACOCF3 completely inhibited prostaglandin E2 production induced by endothelin 1 in cultured rat mesangial cells, suggesting that phospholipase A2 is a critical enzyme in this process. Quinacrine 32-41 phospholipase A2 group IB Rattus norvegicus 4-20 8836147-6 1996 The presence of quinacrine, an antagonist of PLA2, during the membrane pretreatment inhibited their fusogenic activity, suggesting the importance of activation of PLA2. Quinacrine 16-26 phospholipase A2 group IB Rattus norvegicus 163-167 8943700-8 1996 The kinetics of the time dependent docosahexaenoic acid release and the effects of quinacrine suggest that this release is mediated in part by activation of phospholipase A2. Quinacrine 83-93 phospholipase A2 group IB Rattus norvegicus 157-173 8786557-3 1996 In this study, we have investigated whether PLA2 inhibition, by quinacrine, has any effects on stimulant-induced behavioral sensitization. Quinacrine 64-74 phospholipase A2 group IB Rattus norvegicus 44-48 21153096-4 1996 From enzymatic assays, phospholipase A(2) and diacylglycerol lipase were activated by carbamylcholine and these activations were inhibited by the phospholipase A(2) inhibitors, mepacrine and aristolochic acid, and by the diacylglycerol lipase inhibitor RHC 80267. Quinacrine 177-186 phospholipase A2 group IB Rattus norvegicus 23-67 8781605-3 1996 Several recent reports have shown that quinacrine, besides being a potent inhibitor of PLA2, suppresses the generation of ODFR. Quinacrine 39-49 phospholipase A2 group IB Rattus norvegicus 87-91 8621160-8 1996 Moreover, a commonly used phospholipase A2 (PLA2) inhibitor, quinacrine, decreased HGF-induced [3H]AA release and [3H]thymidine incorporation. Quinacrine 61-71 phospholipase A2 group IB Rattus norvegicus 26-42 8621160-8 1996 Moreover, a commonly used phospholipase A2 (PLA2) inhibitor, quinacrine, decreased HGF-induced [3H]AA release and [3H]thymidine incorporation. Quinacrine 61-71 phospholipase A2 group IB Rattus norvegicus 44-48 8640337-18 1995 The phospholipase A2 inhibitor, quinacrine (up to 100 microM) also blocked the effect of acetylcholine on the outflow of 3H-prostaglandins, but this was not followed by a compensatory increase in the outflow of [3H]-arachidonic acid. Quinacrine 32-42 phospholipase A2 group IB Rattus norvegicus 4-20 8779929-6 1996 The PLA2 inhibitors quinacrine (1 microM), aristolochic acid (250 microM), and octadecylbenzoylacrylic acid (7 microM) inhibited BK channels by 61 +/- 6, 47 +/- 2, and 30 +/- 9%, respectively, and in a manner indistinguishable from general anesthetics inhibition. Quinacrine 20-30 phospholipase A2 group IB Rattus norvegicus 4-8 7784893-3 1995 In the present work, it was demonstrated that pretreatment of rats with PLA2 inhibitor, quinacrine (20 mg/kg, I.P. Quinacrine 88-98 phospholipase A2 group IB Rattus norvegicus 72-76 8529043-6 1995 Mepacrine, a PLA2 inhibitor, reversed the pump effect of all agents, and arachidonic acid (AA) produced a dose-dependent pump inhibition, in all three nephron segments. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 13-17 7759504-6 1995 Similarly, when the GH-induced liberation of [3H]AA was blocked by the PLA2 inhibitor mepacrine or the Ca2+ channel blocker verapamil, GH-induced accumulation of P4502C12 mRNA was absent. Quinacrine 86-95 phospholipase A2 group IB Rattus norvegicus 71-75 7753489-2 1995 In comparison with the control group, the phospholipase A2 inhibitor mepacrine significantly decreased the ischemia-evoked efflux of transmitter amino acids into cortical superfusates. Quinacrine 69-78 phospholipase A2 group IB Rattus norvegicus 42-58 8537304-6 1995 The stimulatory effect of mastoparan was little affected in cells that had been treated with pertussis toxin, but it was strongly suppressed in the presence of quinacrine, an inhibitor of phospholipase A2. Quinacrine 160-170 phospholipase A2 group IB Rattus norvegicus 188-204 7537492-5 1995 On the other hand, the presence of EGTA or 100 microM quinacrine, an inhibitor of PLA2, during treatment of plasma membranes with PLA2 inhibited their fusogenic activity, suggesting the importance of activation of PLA2. Quinacrine 54-64 phospholipase A2 group IB Rattus norvegicus 82-86 7537492-5 1995 On the other hand, the presence of EGTA or 100 microM quinacrine, an inhibitor of PLA2, during treatment of plasma membranes with PLA2 inhibited their fusogenic activity, suggesting the importance of activation of PLA2. Quinacrine 54-64 phospholipase A2 group IB Rattus norvegicus 130-134 7537492-5 1995 On the other hand, the presence of EGTA or 100 microM quinacrine, an inhibitor of PLA2, during treatment of plasma membranes with PLA2 inhibited their fusogenic activity, suggesting the importance of activation of PLA2. Quinacrine 54-64 phospholipase A2 group IB Rattus norvegicus 130-134 7900800-3 1995 Treatment with a PLA2 inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA2 activity and abrogated subsequent PMN priming and lung leak (P < 0.05). Quinacrine 33-43 phospholipase A2 group IB Rattus norvegicus 17-21 7900800-3 1995 Treatment with a PLA2 inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA2 activity and abrogated subsequent PMN priming and lung leak (P < 0.05). Quinacrine 33-43 phospholipase A2 group IB Rattus norvegicus 103-107 7900800-4 1995 However, when quinacrine was administered after 2 h of reperfusion, circulating PMN priming and lung leak continued to evolve despite suppression of intestinal PLA2 activity. Quinacrine 14-24 phospholipase A2 group IB Rattus norvegicus 160-164 8001364-12 1995 CONCLUSIONS: The observation that quinacrine and preshock diltiazem limited the extent of shock-induced mucosal injury and bacterial translocation indicate that calcium and phospholipase A2 are involved in the pathogenesis of shock-induced mucosal injury and bacterial translocation. Quinacrine 34-44 phospholipase A2 group IB Rattus norvegicus 173-189 7713816-1 1995 Mepacrine, a cell membrane stabilizer and inhibitor of phospholipase A2 (PLA2), exerts a protective effect on ischemia-reperfusion injury in heart; however, its effect in lungs has not been examined. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 55-71 7713816-1 1995 Mepacrine, a cell membrane stabilizer and inhibitor of phospholipase A2 (PLA2), exerts a protective effect on ischemia-reperfusion injury in heart; however, its effect in lungs has not been examined. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 73-77 7713816-10 1995 This protective effect of mepacrine may not be the result of its inhibition of PLA2 but rather of its downregulation of oxygen radical production by circulating or resident leukocytes or its attenuation of TNF-alpha production by macrophages. Quinacrine 26-35 phospholipase A2 group IB Rattus norvegicus 79-83 8039843-7 1994 The synthesis of vasoconstrictor prostaglandins, such as thromboxane A2, may be stimulated during acetylcholine treatment, resulting in the attenuation of acetylcholine relaxation, because the relaxation was abolished by treatment with the phospholipase A2 inhibitor quinacrine, cyclooxygenase inhibitor indomethacin, prostaglandin H2/thromboxane A2 receptor antagonist S1452, and thromboxane A2 synthase inhibitor dazmegrel. Quinacrine 267-277 phospholipase A2 group IB Rattus norvegicus 240-256 7889312-11 1994 This EDHF-type dilation was reversibly inhibited by the phospholipase A2 inhibitor, quinacrine (3 microM, 9 +/- 3% decrease in CPP, n = 6, P < 0.01) and by the cytochrome P450 inhibitor SKF525a (3 microM, 6 +/- 1% decrease in CPP, n = 6, P < 0.01). Quinacrine 84-94 phospholipase A2 group IB Rattus norvegicus 56-72 7918869-3 1994 This response could be fully prevented by pretreatment of cells with the PLA2 inhibitor, mepacrine. Quinacrine 89-98 phospholipase A2 group IB Rattus norvegicus 73-77 8135755-5 1994 This hypothesis was confirmed by finding that both Ang II-induced 6-oxo-PGF1 alpha production and ANP release were abolished in the presence of the respective phospholipase A2 and cyclo-oxygenase inhibitors quinacrine (10 microM) and indomethacin (10 microM), whereas exogenously applied PGI2 (1 microM) and prostaglandin E2 (0.1 microM) mimicked Ang II-induced ANP secretion in this system. Quinacrine 207-217 phospholipase A2 group IB Rattus norvegicus 159-175 7918869-7 1994 The effect was inhibited by mepacrine, further supporting the pivotal role of PLA2 in the release of the eicosanoid precursor, AA. Quinacrine 28-37 phospholipase A2 group IB Rattus norvegicus 78-82 8122272-7 1994 The PLA2 inhibitors dibucaine (50 microM) and mepacrine (50 microM) inhibited KCN-mediated [3H]AA release. Quinacrine 46-55 phospholipase A2 group IB Rattus norvegicus 4-8 7982028-5 1994 This effect was inhibited by MK-801 and quinacrine, suggesting an involvement of NMDA receptors and phospholipase A2. Quinacrine 40-50 phospholipase A2 group IB Rattus norvegicus 100-116 8227189-6 1993 Quinacrine, a phospholipase A2 inhibitor, significantly suppressed the vasopressin-induced arachidonic acid release but had little effect on the formation of inositol phosphates. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-30 8378085-4 1993 This stimulation was significantly inhibited by mepacrine, a phospholipase A2 (PLA2) inhibitor. Quinacrine 48-57 phospholipase A2 group IB Rattus norvegicus 61-77 8378085-4 1993 This stimulation was significantly inhibited by mepacrine, a phospholipase A2 (PLA2) inhibitor. Quinacrine 48-57 phospholipase A2 group IB Rattus norvegicus 79-83 8429273-5 1993 The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion. Quinacrine 38-48 phospholipase A2 group IB Rattus norvegicus 4-20 8496167-6 1993 Addition of phospholipase A2 (PLA2) inhibitors (quinacrine, 4-bromophenacyl bromide, manoalide) to the perfusion medium inhibited K(+)-stimulated [3H]ACh and [3H]AA release in a dose-dependent manner. Quinacrine 48-58 phospholipase A2 group IB Rattus norvegicus 12-28 8496167-6 1993 Addition of phospholipase A2 (PLA2) inhibitors (quinacrine, 4-bromophenacyl bromide, manoalide) to the perfusion medium inhibited K(+)-stimulated [3H]ACh and [3H]AA release in a dose-dependent manner. Quinacrine 48-58 phospholipase A2 group IB Rattus norvegicus 30-34 8388321-3 1993 Eicosanoid generation is attributable to PLA2 activation since pretreatment with PLA2 irreversible inhibitors, such as mepacrine or para-bromophenacylbromide (pBPB), completely blocks AA metabolite generation. Quinacrine 119-128 phospholipase A2 group IB Rattus norvegicus 41-45 8388321-3 1993 Eicosanoid generation is attributable to PLA2 activation since pretreatment with PLA2 irreversible inhibitors, such as mepacrine or para-bromophenacylbromide (pBPB), completely blocks AA metabolite generation. Quinacrine 119-128 phospholipase A2 group IB Rattus norvegicus 81-85 8388321-5 1993 Treatment of effector cells with mepacrine or pBPB resulted in complete, irreversible, dose-dependent inhibition of both NK and ADCC activities, which were completely reversed by the addition of exogenous PLA2 or its hydrolysis products, AA and lysophosphatidylcholine (lysoPC). Quinacrine 33-42 phospholipase A2 group IB Rattus norvegicus 205-209 8491398-8 1993 Inflamed tissue treated with a phospholipase A2 inhibitor (mepacrine) produced less PGE2, LTD4, and electrical responses when compared with inflamed tissue, either untreated (91%, 92%, and 79% respectively) or treated with cyclo-oxygenase and lipoxygenase inhibition. Quinacrine 59-68 phospholipase A2 group IB Rattus norvegicus 31-47 8464709-2 1993 Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 59-63 8500985-9 1993 Mepacrine, a phospholipase A2 inhibitor, completely inhibited PGD2 and LTC4/D4 generation, as well as AA release itself, without affecting serotonin release. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 13-29 8450566-5 1993 Treatment of cells with the phospholipase A2 inhibitor mepacrine (30 microM) inhibited basal (by 50%) and IL-1 stimulated (by 80%) NGF secretion. Quinacrine 55-64 phospholipase A2 group IB Rattus norvegicus 28-44 8429273-5 1993 The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion. Quinacrine 38-48 phospholipase A2 group IB Rattus norvegicus 22-26 8429273-5 1993 The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion. Quinacrine 38-48 phospholipase A2 group IB Rattus norvegicus 152-156 1848278-9 1991 Moreover, the inhibitory effect of 8-OH-DPAT on the carbachol response was blocked by 10 microM quinacrine (a phospholipase A2 inhibitor) but not by BW 755C (100 microM), a cyclooxygenase and lipoxygenase inhibitor. Quinacrine 96-106 phospholipase A2 group IB Rattus norvegicus 110-126 1330464-2 1992 The phospholipase A2 inhibitor mepacrine at 25 and 50 mumol/l significantly inhibited glucagon secretion induced by 0.1 mumol/l clonidine (P less than 0.01, respectively), whereas 5 mumol/l mepacrine did not affect clonidine-induced glucagon secretion. Quinacrine 31-40 phospholipase A2 group IB Rattus norvegicus 4-20 1332181-2 1992 Phospholipase A2 (PLA2) stimulated PRL secretion, while the PLA2 inhibitor quinacrine reduced both thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated PRL release. Quinacrine 75-85 phospholipase A2 group IB Rattus norvegicus 60-64 1349027-6 1992 To verify whether the mechanism of pump inhibition by agents that increase cell cAMP involves phospholipase A2 (PLA2), we used mepacrine, a PLA2 inhibitor, which also abolished Na-K-ATPase inhibition by DA or fenoldopam, as well as by AVP, forskolin, or dBcAMP. Quinacrine 127-136 phospholipase A2 group IB Rattus norvegicus 94-110 1349027-6 1992 To verify whether the mechanism of pump inhibition by agents that increase cell cAMP involves phospholipase A2 (PLA2), we used mepacrine, a PLA2 inhibitor, which also abolished Na-K-ATPase inhibition by DA or fenoldopam, as well as by AVP, forskolin, or dBcAMP. Quinacrine 127-136 phospholipase A2 group IB Rattus norvegicus 112-116 1349027-6 1992 To verify whether the mechanism of pump inhibition by agents that increase cell cAMP involves phospholipase A2 (PLA2), we used mepacrine, a PLA2 inhibitor, which also abolished Na-K-ATPase inhibition by DA or fenoldopam, as well as by AVP, forskolin, or dBcAMP. Quinacrine 127-136 phospholipase A2 group IB Rattus norvegicus 140-144 1373616-1 1992 In intact rat pancreatic acini, the phospholipase A2 inhibitor mepacrine did not affect basal amylase release but dose-dependently inhibited the carbachol (IC50 65 microM) and CCK-8 (IC50 210 microM)-stimulated amylase release. Quinacrine 63-72 phospholipase A2 group IB Rattus norvegicus 36-52 1355446-5 1992 NMDA-evoked arachidonic acid release was inhibited by MK-801 and TCP (two NMDA receptor-type antagonists), or by mepacrine, an inhibitor of phospholipase A2. Quinacrine 113-122 phospholipase A2 group IB Rattus norvegicus 140-156 1721808-2 1991 Mepacrine, a known inhibitor of phospholipase A2, at concentrations below 10(-5) M and anti-rat 14-kDa group II phospholipase A2 antibody inhibited histamine release, while they did not affect the prostaglandin generation. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 32-48 1667913-8 1991 Quinacrine (phospholipase A2 inhibitor), indomethacin (cyclooxygenase inhibitor) and nordihydroguaiaretic acid (NDGA, lipoxygenase inhibitor) potentiated the relaxation induced by emodin. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 12-28 1951711-4 1991 The synergistic effect was dose dependent (maximal at 1 nM) and due to enhanced gene expression, since the cytokine treatment caused a fivefold increase in NGF mRNA after 8 h. Stimulation of NGF synthesis was abolished by mepacrine and dexamethasone, indicating that phospholipase A2 may be involved in NGF regulation. Quinacrine 222-231 phospholipase A2 group IB Rattus norvegicus 267-283 1944607-2 1991 In the preparation with the submucosal plexus, quinacrine and indomethacin completely blocked the effect of melittin, indicating activation of phospholipase A2 and production of prostaglandins induced by the drug. Quinacrine 47-57 phospholipase A2 group IB Rattus norvegicus 143-159 1944607-8 1991 The results provide evidence for the presence of a quinacrine-sensitive phospholipase A2 in the preparation with and that without the submucosa. Quinacrine 51-61 phospholipase A2 group IB Rattus norvegicus 72-88 1646955-5 1991 On the other hand, the L(+)-lactate-evoked supersensitivity could be blocked by the phospholipase A2 inhibitors mepacrine and n-bromophenacyl-bromide, suggesting an involvement of phospholipase A2 in the process of beta-adrenergic sensitization. Quinacrine 112-121 phospholipase A2 group IB Rattus norvegicus 84-100 1646955-5 1991 On the other hand, the L(+)-lactate-evoked supersensitivity could be blocked by the phospholipase A2 inhibitors mepacrine and n-bromophenacyl-bromide, suggesting an involvement of phospholipase A2 in the process of beta-adrenergic sensitization. Quinacrine 112-121 phospholipase A2 group IB Rattus norvegicus 180-196 1396679-8 1992 The effect of thrombin on carbohydrate output was also blocked by a phospholipase A2 inhibitor (quinacrine, 50 microM) and by an inhibitor of the cyclooxygenase (indomethacin, 20 microM), suggesting the involvement of cyclooxygenase in the mechanism of action of thrombin. Quinacrine 96-106 phospholipase A2 group IB Rattus norvegicus 68-84 1382129-2 1992 We evaluated the cardioprotective activity of two putative PLA2 inhibitors, quinacrine and 7,7-dimethyleicosadienoic acid (DEDA), in isolated globally ischemic rat hearts. Quinacrine 76-86 phospholipase A2 group IB Rattus norvegicus 59-63 1386368-6 1992 The phospholipase A2 inhibitor, mepacrine, had no effect on AVP-mediated AA release, but abolished the synergistic action of EGF-URO. Quinacrine 32-41 phospholipase A2 group IB Rattus norvegicus 4-20 1322564-3 1992 METHODS: Sprague-Dawley rats were pretreated with a PLA2 inhibitor, quinacrine (10 mg/kg, intravenously), before the induction of gut ischemia (45 minutes of superior mesenteric artery occlusion) followed by 6 hours of reperfusion. Quinacrine 68-78 phospholipase A2 group IB Rattus norvegicus 52-56 1327821-10 1992 The dilator activity of scoparone was also inhibited by quinacrine (inhibitor of phospholipase A2) and indomethacin (inhibitor of cyclooxygenase). Quinacrine 56-66 phospholipase A2 group IB Rattus norvegicus 81-97 1382379-2 1992 Injection of phospholipase A2 (PLA2) in the rat skin produced a significant rise in oedema, which was inhibited by the simultaneous coinjection of aristolochic acid (100 micrograms), mepacrine (100 micrograms) and p-bromophenacyl bromide (10 micrograms). Quinacrine 183-192 phospholipase A2 group IB Rattus norvegicus 13-29 1382379-2 1992 Injection of phospholipase A2 (PLA2) in the rat skin produced a significant rise in oedema, which was inhibited by the simultaneous coinjection of aristolochic acid (100 micrograms), mepacrine (100 micrograms) and p-bromophenacyl bromide (10 micrograms). Quinacrine 183-192 phospholipase A2 group IB Rattus norvegicus 31-35 1382379-5 1992 Dose-dependent histamine release by rat peritoneal cells was induced by PLA2 and by lysophosphatidylserine and this effect could be antagonized by aristolochic acid and mepacrine. Quinacrine 169-178 phospholipase A2 group IB Rattus norvegicus 72-76 1427593-8 1992 In Experiment II designed to study the cause of the exercise-induced decrease in PE and PC, intravenous quinacrine was used to inhibit PLA2. Quinacrine 104-114 phospholipase A2 group IB Rattus norvegicus 135-139 1427593-14 1992 These results suggest that quinacrine can partially prevent the decrease of phospholipid and partially inhibit the activity of PLA2 after prolonged exercise. Quinacrine 27-37 phospholipase A2 group IB Rattus norvegicus 127-131 1833985-6 1991 Inhibition of phospholipase A2 (PLA2) activity with quinacrine (100 microM) completely blocked the dopamine-stimulated PGE2 production, whereas inhibition of polyphosphoinositol hydrolysis with neomycin (100 microM) or inhibition of protein kinase C with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (10 microM) did not. Quinacrine 52-62 phospholipase A2 group IB Rattus norvegicus 14-30 1833985-6 1991 Inhibition of phospholipase A2 (PLA2) activity with quinacrine (100 microM) completely blocked the dopamine-stimulated PGE2 production, whereas inhibition of polyphosphoinositol hydrolysis with neomycin (100 microM) or inhibition of protein kinase C with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (10 microM) did not. Quinacrine 52-62 phospholipase A2 group IB Rattus norvegicus 32-36 1910075-3 1991 Quinacrine, an inhibitor of phospholipase A2 (PLA2), suppressed AA release by about 60% and neomycin, a putative inhibitor of phospholipase C (PLC), reduced AA release by about 30%. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 28-44 1910075-3 1991 Quinacrine, an inhibitor of phospholipase A2 (PLA2), suppressed AA release by about 60% and neomycin, a putative inhibitor of phospholipase C (PLC), reduced AA release by about 30%. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 46-50 1659882-8 1991 Similarly, the PLA2 inhibitors quinacrine, dexamethasone and corticosterone, added to the Leydig cells in vitro, inhibited LH-stimulated testosterone production but not cyclic AMP production. Quinacrine 31-41 phospholipase A2 group IB Rattus norvegicus 15-19 1663633-7 1991 Coincubation of C6 cells with either the phospholipase A2 (PLA2) inhibitor mepacrine or the protein kinase C (PKC) inhibitor H7, during chronic treatment with DMI, blocked the down-regulation of beta ARs. Quinacrine 75-84 phospholipase A2 group IB Rattus norvegicus 41-57 1663633-7 1991 Coincubation of C6 cells with either the phospholipase A2 (PLA2) inhibitor mepacrine or the protein kinase C (PKC) inhibitor H7, during chronic treatment with DMI, blocked the down-regulation of beta ARs. Quinacrine 75-84 phospholipase A2 group IB Rattus norvegicus 59-63 2695506-2 1989 This LHRH-A-induced T secretion was completely blocked by quinacrine and chloroquine, inhibitors of phospholipase A2. Quinacrine 58-68 phospholipase A2 group IB Rattus norvegicus 100-116 2090584-4 1990 Hydrogen peroxide-stimulated 6-keto-PGF1 alpha release was blocked (50%) by phospholipase A2 (PLA2) inhibitors quinacrine and dimethyleicosadienoic acid at 5 min. Quinacrine 111-121 phospholipase A2 group IB Rattus norvegicus 76-92 2090584-4 1990 Hydrogen peroxide-stimulated 6-keto-PGF1 alpha release was blocked (50%) by phospholipase A2 (PLA2) inhibitors quinacrine and dimethyleicosadienoic acid at 5 min. Quinacrine 111-121 phospholipase A2 group IB Rattus norvegicus 94-98 1980544-4 1990 The contraction could be blocked by the cyclooxygenase inhibitor indomethacin and the phospholipase A2 inhibitor quinacrine, suggesting a role for prostaglandins in the response. Quinacrine 113-123 phospholipase A2 group IB Rattus norvegicus 86-102 2095437-3 1990 Cumene hydroperoxide-induced damage was reduced or prevented by several compounds: the application of Trolox C, a water-soluble vitamin E analogue, and of phospholipase A2 inhibitors chlorpromazine and (to a lesser extent) quinacrine prevented alpha-HBDH release. Quinacrine 223-233 phospholipase A2 group IB Rattus norvegicus 155-171 2117049-6 1990 Quinacrine, a nonselective phospholipase A2 inhibitor, reduced the carbachol stimulation of adenylate cyclase activity, but this inhibition appeared to be competitive with a Ki of 0.2 microM. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 27-43 2231411-6 1990 However, melittin-stimulated renin secretion is independent of melittin-stimulated phospholipase A2 activity, arachidonic acid release, and PG synthesis, since 20 microM-quinacrine (a phospholipase A2 antagonist) and 50 microM-meclofenamate (a cyclooxygenase antagonist) antagonized basal and melittin-stimulated PGE2 synthesis but had no effects on basal or melittin-stimulated renin secretion. Quinacrine 170-180 phospholipase A2 group IB Rattus norvegicus 184-200 1977095-7 1990 A phospholipase A2 inhibitor (10(-6) M, quinacrine) completely abolished the stimulatory effect of GRF on both AA and SRIF release. Quinacrine 40-50 phospholipase A2 group IB Rattus norvegicus 2-18 2097100-2 1990 In the present study we examined the effect of mepacrine, an inhibitor of phospholipase A2, on lung injury induced by PMA in isolated blood-perfused rat lungs. Quinacrine 47-56 phospholipase A2 group IB Rattus norvegicus 74-90 2108808-2 1990 It seems likely that activation of phospholipase A2 (PLA2) is the mechanism mainly responsible for the rise of cytosolic arachidonate, since the latter is prevented by the PLA2 inhibitors indomethacin and mepacrine. Quinacrine 205-214 phospholipase A2 group IB Rattus norvegicus 35-51 2108808-2 1990 It seems likely that activation of phospholipase A2 (PLA2) is the mechanism mainly responsible for the rise of cytosolic arachidonate, since the latter is prevented by the PLA2 inhibitors indomethacin and mepacrine. Quinacrine 205-214 phospholipase A2 group IB Rattus norvegicus 53-57 2108808-2 1990 It seems likely that activation of phospholipase A2 (PLA2) is the mechanism mainly responsible for the rise of cytosolic arachidonate, since the latter is prevented by the PLA2 inhibitors indomethacin and mepacrine. Quinacrine 205-214 phospholipase A2 group IB Rattus norvegicus 172-176 1703978-4 1990 This enhancement of the release of radioactivity was inhibited by phospholipase A2 inhibitors, quinacrine (1 mM) and p-bromophenacyl bromide (10 microM), suggesting that polyethylenimine and polyallylamine activates phospholipase A2 to generate arachidonate and its metabolites. Quinacrine 95-105 phospholipase A2 group IB Rattus norvegicus 66-82 1703978-4 1990 This enhancement of the release of radioactivity was inhibited by phospholipase A2 inhibitors, quinacrine (1 mM) and p-bromophenacyl bromide (10 microM), suggesting that polyethylenimine and polyallylamine activates phospholipase A2 to generate arachidonate and its metabolites. Quinacrine 95-105 phospholipase A2 group IB Rattus norvegicus 216-232 2299401-8 1990 The phospholipase A2 inhibitors quinacrine hydrochloride, trifluoperazine, and 4-bromophenacylbromide dose-dependently inhibited potassium depolarization-induced activation of specific 3H-HCh-3 binding in slices of rat brain in vitro. Quinacrine 32-56 phospholipase A2 group IB Rattus norvegicus 4-20 2314485-5 1990 Phospholipase A2 inhibitors such as quinacrine and ONO-RS-082 abolished the relaxation induced by ACh but did not affect that by PAF. Quinacrine 36-46 phospholipase A2 group IB Rattus norvegicus 0-16 2128375-3 1990 We found that, in normal skin, bradykinin hyperalgesia is inhibited by the phospholipase A2 inhibitor, mepacrine, but not by the phospholipase C inhibitor, neomycin and is mimicked by phospholipase A2. Quinacrine 103-112 phospholipase A2 group IB Rattus norvegicus 75-91 2570849-1 1989 p-Bromophenacyl bromide (PBPB), quinacrine and indomethacin, which inhibit phospholipase A2 (PLA2; EC 3.1.1.4) activity in several tissues, caused a dose-dependent inhibition of prelabelled [3H]noradrenaline ([3H]NA) release evoked by high concentrations of K+ from rat cerebral cortical synaptosomes. Quinacrine 32-42 phospholipase A2 group IB Rattus norvegicus 75-91 2570849-1 1989 p-Bromophenacyl bromide (PBPB), quinacrine and indomethacin, which inhibit phospholipase A2 (PLA2; EC 3.1.1.4) activity in several tissues, caused a dose-dependent inhibition of prelabelled [3H]noradrenaline ([3H]NA) release evoked by high concentrations of K+ from rat cerebral cortical synaptosomes. Quinacrine 32-42 phospholipase A2 group IB Rattus norvegicus 93-97 2551803-3 1989 Pretreatment of animals with quinacrine, a known inhibitor of phospholipase A2, prevented the increases in the luminal N-acetyl-beta-glucosaminidase activity, mucosal permeability, malondialdehyde and myeloperoxidase activity after deposition of phospholipase C in the gut lumen. Quinacrine 29-39 phospholipase A2 group IB Rattus norvegicus 62-78 2551803-5 1989 Part of its action may be mediated via phospholipase A2 activation since pretreatment with quinacrine afforded protection. Quinacrine 91-101 phospholipase A2 group IB Rattus norvegicus 39-55 2128431-3 1990 Quinacrine, inhibitor of phospholipase A2 (PLA2), suppressed AA release by 60% and neomycin, inhibitor of phospholipase C (PLC) by about 30%. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 25-41 2128431-3 1990 Quinacrine, inhibitor of phospholipase A2 (PLA2), suppressed AA release by 60% and neomycin, inhibitor of phospholipase C (PLC) by about 30%. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 43-47 2482349-7 1989 p-Bromophenacyl bromide and mepacrine, PLA2 inhibitors, inhibited the release of histamine caused by PLA2. Quinacrine 28-37 phospholipase A2 group IB Rattus norvegicus 39-43 2482349-7 1989 p-Bromophenacyl bromide and mepacrine, PLA2 inhibitors, inhibited the release of histamine caused by PLA2. Quinacrine 28-37 phospholipase A2 group IB Rattus norvegicus 101-105 2542466-7 1989 A role for phospholipase A2 is also possible, because pretreatment of cultures with quinacrine partially blocked arachidonic acid release. Quinacrine 84-94 phospholipase A2 group IB Rattus norvegicus 11-27 2542410-7 1989 Treatment of cells with phospholipase A2 inhibitors, mepacrine and bromophenacyl bromide, abolished AA release by C5b-9. Quinacrine 53-62 phospholipase A2 group IB Rattus norvegicus 24-40 2495005-1 1989 In view of the fact that mepacrine (Mp) is usually used as an inhibitor of the endogenous phospholipase A2, and since this enzyme produces the release of arachidonic acid (AA) from membrane phospholipids, we studied the effect of different concentrations of Mp on the mobilization of [1-14C]AA in rat renomedullary phospholipids. Quinacrine 25-34 phospholipase A2 group IB Rattus norvegicus 90-106 2495005-1 1989 In view of the fact that mepacrine (Mp) is usually used as an inhibitor of the endogenous phospholipase A2, and since this enzyme produces the release of arachidonic acid (AA) from membrane phospholipids, we studied the effect of different concentrations of Mp on the mobilization of [1-14C]AA in rat renomedullary phospholipids. Quinacrine 36-38 phospholipase A2 group IB Rattus norvegicus 90-106 2543618-9 1989 Quinacrine, a phospholipase A2 inhibitor, suppressed the incorporation of [32P]Pi into this phospholipid on dose dependently. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-30 2920033-3 1989 When PlA2 was inhibited with chlorpromazine, mepacrine, or p-bromphenacyl bromide, the accumulation of thiobarbituric acid reactive substances (TBARS) was reduced in a dose dependent manner. Quinacrine 45-54 phospholipase A2 group IB Rattus norvegicus 5-9 3164726-15 1988 This evidence, together with inhibition of acylhydrolase activity with phospholipase A2 inhibitors, dibucaine and mepacrine, indicates that the primary acylhydrolase activity was due to phospholipase A2. Quinacrine 114-123 phospholipase A2 group IB Rattus norvegicus 186-202 2570543-11 1989 Results obtained with the phospholipase A-2 inhibitor mepacrine and the acyltransferase inhibitor THC suggest that NE attenuates PL acylation by activating phospholipase A-2, but it concomitantly enhances PI acylation by selectively stimulating a PI-specific arachidonyl transferase via mechanisms that have not yet been elucidated. Quinacrine 54-63 phospholipase A2 group IB Rattus norvegicus 26-43 3143415-4 1988 Evidence for LPS activation of phospholipase A2 included a time-dependent LPS-induced generation of [32P]lysophosphatidylcholine and the inhibitory effects of a phospholipase A2 inhibitor, mepacrine, on LPS-induced PGE2 formation. Quinacrine 189-198 phospholipase A2 group IB Rattus norvegicus 31-47 3143415-4 1988 Evidence for LPS activation of phospholipase A2 included a time-dependent LPS-induced generation of [32P]lysophosphatidylcholine and the inhibitory effects of a phospholipase A2 inhibitor, mepacrine, on LPS-induced PGE2 formation. Quinacrine 189-198 phospholipase A2 group IB Rattus norvegicus 161-177 3218612-0 1988 Quinacrine prevention of intestinal ischaemic mucosal damage is partly mediated through inhibition of intraluminal phospholipase A2. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 115-131 3218612-4 1988 Pretreatment of animals with the phospholipase A2 inhibitor, quinacrine prevented the increases in luminal phospholipase A2 activity and mucosal damage following ischaemia and revascularization. Quinacrine 61-71 phospholipase A2 group IB Rattus norvegicus 33-49 3218612-4 1988 Pretreatment of animals with the phospholipase A2 inhibitor, quinacrine prevented the increases in luminal phospholipase A2 activity and mucosal damage following ischaemia and revascularization. Quinacrine 61-71 phospholipase A2 group IB Rattus norvegicus 107-123 3218612-6 1988 Again, quinacrine pretreatment of animals prevented the increases in mucosal permeability and activity of N-acetyl-beta-glucosaminidase after intraluminal injection of purified phospholipase A2. Quinacrine 7-17 phospholipase A2 group IB Rattus norvegicus 177-193 2447244-4 1988 The effect of PLA2 was prevented by EGTA and two nonselective PLA2 inhibitors, mepacrine and bromophenacyl bromide. Quinacrine 79-88 phospholipase A2 group IB Rattus norvegicus 14-18 3335042-1 1988 Mammary carcinogenesis studies were conducted to determine the chemopreventive activity of quinacrine, an antimalarial drug which suppresses the production of arachidonic acid from phospholipid through inhibition of phospholipase A2. Quinacrine 91-101 phospholipase A2 group IB Rattus norvegicus 216-232 2830996-3 1988 All these effects were efficiently inhibited by the PLA2 inhibitor quinacrine. Quinacrine 67-77 phospholipase A2 group IB Rattus norvegicus 52-56 2838694-3 1988 Similar inhibitory effects are observed with mepacrine, an inhibitor of phospholipase A2 (PLA2). Quinacrine 45-54 phospholipase A2 group IB Rattus norvegicus 72-88 2838694-3 1988 Similar inhibitory effects are observed with mepacrine, an inhibitor of phospholipase A2 (PLA2). Quinacrine 45-54 phospholipase A2 group IB Rattus norvegicus 90-94 3428670-3 1987 Pretreatment with the phospholipase A2 inhibitor, quinacrine, prevented the increases in mucosal phospholipase A2 activity and lysophosphatidylcholine/phosphatidylcholine ratio after ischaemia and morphological examinations revealed that the mucosa was then also protected against ischaemic injury. Quinacrine 50-60 phospholipase A2 group IB Rattus norvegicus 22-38 3428670-3 1987 Pretreatment with the phospholipase A2 inhibitor, quinacrine, prevented the increases in mucosal phospholipase A2 activity and lysophosphatidylcholine/phosphatidylcholine ratio after ischaemia and morphological examinations revealed that the mucosa was then also protected against ischaemic injury. Quinacrine 50-60 phospholipase A2 group IB Rattus norvegicus 97-113 3120519-5 1987 Quinacrine, a non specific inhibitor of phospholipase A2 impaired PAF-acether formation in a dose-dependent manner. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 40-56 3119146-3 1987 This effect was inhibited by the protein kinase inhibitor 1-(-5-isoquinolinylsulfonyl)-2-methylpiperizine (IC50 = 25 microM) and the phospholipase A2 inhibitor, mepacrine (IC50 = 5 microM). Quinacrine 161-170 phospholipase A2 group IB Rattus norvegicus 133-149 3120703-6 1987 A transient appearance of radiolabelled phosphatidic acid and diacylglycerol indicated phosphatidylinositol hydrolysis by phospholipase C. Pretreatment with a phospholipase A2 inhibitor, mepacrine, substantially prevented the antigen-induced liberation of [3H]arachidonic acid from phosphatidylcholine. Quinacrine 187-196 phospholipase A2 group IB Rattus norvegicus 159-175 3879308-4 1985 Quinacrine, a phospholipase A2 inhibitor, methylene blue, a guanylate cyclase inhibitor and tetraethylammonium, a potassium permeability inhibitor, inhibited carbachol-induced relaxation and augmented the magnitude of norepinephrine-induced contraction only when endothelium was present. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 14-30 3553641-5 1986 PG I2 synthesis by rat aortic ring was inhibited by mepacrine, which inhibits phospholipase A2. Quinacrine 52-61 phospholipase A2 group IB Rattus norvegicus 78-94 3455595-11 1986 was inhibitory at 10(-5) M and showed no effects at 10(-6) M. However, after washing quinacrine, normal elongation rate was recovered by those previously treated with 10(-5) M and axon growth was enhanced in those treated with 10(-6) M. Since three different phospholipase A2 inhibitors, tested in different situations, produce a similar biphasic effect on axon elongation rate, we postulate that this enzymatic activity is involved in the motility of axon growth cones. Quinacrine 85-95 phospholipase A2 group IB Rattus norvegicus 259-275 3102257-2 1986 Mepacrine, a phospholipase A2 inhibitor (3 X 10(-5) M) and the lipoxygenase inhibitor nordihydroguaiaretic acid (10(-5) M) inhibited this response whereas the cyclooxygenase inhibitor, diclofenac sodium (10(-5) M), and the thromboxane synthetase inhibitor imidazole (10(-5) M) did not. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 13-29 3709328-7 1986 In contrast, indomethacin (5 mg/kg) and aspirin (200 mg/kg) as cyclooxygenase inhibitors or quinacrine (100 mg/kg) as a phospholipase A2 inhibitor significantly decreased both the pH and acid neutralizing capacity. Quinacrine 92-102 phospholipase A2 group IB Rattus norvegicus 120-136 3015753-7 1986 Mepacrine, a phospholipase A2 inhibitor, strongly inhibited it. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 13-29 2578123-3 1985 For verapamil, diltiazem, trifluoperazine, dibucaine, and quinacrine, there is complete agreement between the relative potencies as inhibitors of phospholipase A2 and the two other processes. Quinacrine 58-68 phospholipase A2 group IB Rattus norvegicus 146-162 3924121-2 1985 The effect of melittin on insulin secretion was dependent on extracellular calcium, was inhibited by the phospholipase A2 inhibitor quinacrine and by the lipoxygenase inhibitor nordihydroguaiaretic acid. Quinacrine 132-142 phospholipase A2 group IB Rattus norvegicus 105-121 2981387-4 1985 Quinacrine antagonized the stimulatory effects of ouabain, vanadate, and K-free medium on prostaglandin E2 release (consistent with phospholipase A2 involvement), but did not antagonize their inhibitory effects on renin secretion. Quinacrine 0-10 phospholipase A2 group IB Rattus norvegicus 132-148 6354779-6 1983 These glucose-induced increases in 3H-arachidonic acid-derived radioactivity in both the phospholipid and the prostaglandin fractions were eliminated by the inhibition of phospholipase A2 activity with mepacrine or by the inhibition of cyclooxygenase activity with sodium salicylate. Quinacrine 202-211 phospholipase A2 group IB Rattus norvegicus 171-187 20493019-2 1985 Chloroquine and quinacrine, which block the action of phospholipase A(2), inhibited either the phospholipase A(2)-stimulated or the high potassium-stimulated release of [(3)H]norepinephrine from synaptosomes. Quinacrine 16-26 phospholipase A2 group IB Rattus norvegicus 54-72 20493019-2 1985 Chloroquine and quinacrine, which block the action of phospholipase A(2), inhibited either the phospholipase A(2)-stimulated or the high potassium-stimulated release of [(3)H]norepinephrine from synaptosomes. Quinacrine 16-26 phospholipase A2 group IB Rattus norvegicus 95-113 6383404-2 1984 The phospholipase A2 was activated by Ca2+ (Ka approximately 0.5 mM) and inhibited by mepacrine. Quinacrine 86-95 phospholipase A2 group IB Rattus norvegicus 4-20 6088738-5 1984 These changes in beta-adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor. Quinacrine 72-82 phospholipase A2 group IB Rattus norvegicus 86-102 6147931-3 1984 Mepacrine, a phospholipase A2 inhibitor, suppressed the generation of both leukotrienes (SRS) and prostaglandins (PG), whereas the lipoxygenase inhibitor BW 755C reduced the generation of SRS, and the cyclooxygenase inhibitor indomethacin significantly suppressed the generation of PG. Quinacrine 0-9 phospholipase A2 group IB Rattus norvegicus 13-29 6887013-2 1983 In the heart, the phospholipase A2 inhibitor mepacrine (10(-4) M) reduced the choline efflux (1.1 nmol g-1 min-1) by 51 +/- 5% (N = 3), whereas several cholinesterase inhibitors (physostigmine, neostigmine and diisopropylfluorophosphate) and muscarinic agonists (acetylcholine, oxotremorine and bethanechol) caused an increase. Quinacrine 45-54 phospholipase A2 group IB Rattus norvegicus 18-34 6859870-5 1983 Increased lysophosphatidylcholine formation was evident following lipid peroxidation in phospholipase A2-containing liposomes which was inhibited by p-bromophenacyl bromide and mepacrine. Quinacrine 177-186 phospholipase A2 group IB Rattus norvegicus 88-104 28129740-3 2017 In the present study an attempt was made to investigate the effect of quinacrine, a phospholipase A2 inhibitor against glycerol induced AKI in rats. Quinacrine 70-80 phospholipase A2 group IB Rattus norvegicus 84-100 6297604-5 1983 Exposure of isolated type II cells to the phospholipase A2 inhibitors 4-bromophenacylbromide or quinacrine dihydrochloride led to a decreased synthesis of total phosphatidylcholines from various labelled precursors. Quinacrine 96-122 phospholipase A2 group IB Rattus norvegicus 42-58 6112882-8 1981 Daily injection of quinacrine (16 mg/kg), an antimalarial agent that inhibits phospholipase A2, blocked the subsensitivity to the chronotropic effect of epinephrine, but not that to the pressor effect of epinephrine. Quinacrine 19-29 phospholipase A2 group IB Rattus norvegicus 78-94 6258719-6 1981 Interference with the metabolism of phospholipids by exposure to phospholipase A2 inhibitor, mepacrine (quinacrine), prevents agonist-induced desensitization of beta-adrenoceptors in astrocytoma cells. Quinacrine 93-102 phospholipase A2 group IB Rattus norvegicus 65-81 6258719-6 1981 Interference with the metabolism of phospholipids by exposure to phospholipase A2 inhibitor, mepacrine (quinacrine), prevents agonist-induced desensitization of beta-adrenoceptors in astrocytoma cells. Quinacrine 104-114 phospholipase A2 group IB Rattus norvegicus 65-81 6257888-3 1981 These changes in beta adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor, although the drug had no effect on beta adrenoceptors when given alone. Quinacrine 72-82 phospholipase A2 group IB Rattus norvegicus 86-102 7138896-4 1982 Contrary to previous reports, a biphasic modulatory role of mepacrine on phospholipase A2 activity and platelet aggregation was demonstrated. Quinacrine 60-69 phospholipase A2 group IB Rattus norvegicus 73-89 6807980-10 1982 Indomethacin and aspirin, which inhibit the cyclooxygenase, and mepacrine, which inhibits the Ca2+-activated phospholipase A2, markedly reduced the increase in prostaglandin production. Quinacrine 64-73 phospholipase A2 group IB Rattus norvegicus 109-125 6284950-4 1982 In the present study the effects of reported inhibitors of phospholipase A2 (quinacrine, chlorpromazine, dexamethasone, and dibutyryl cyclic AMP) on diethyl maleate (DEM)-induced lipid peroxidation, reduced glutathione (GSH) depletion, and cellular injury were examined in isolated hepatocyte suspensions. Quinacrine 77-87 phospholipase A2 group IB Rattus norvegicus 59-75 28129740-12 2017 CONCLUSION: The reversal of glycerol induced AKI by quinacrine points towards a role of phospholipase A2 (PLA2) in the pathogenesis of renal injury. Quinacrine 52-62 phospholipase A2 group IB Rattus norvegicus 88-104 28129740-12 2017 CONCLUSION: The reversal of glycerol induced AKI by quinacrine points towards a role of phospholipase A2 (PLA2) in the pathogenesis of renal injury. Quinacrine 52-62 phospholipase A2 group IB Rattus norvegicus 106-110 26076928-6 2015 In L-NAME-treated hearts, 5-HT-induced coronary flow increases were blocked by the phospholipase A2 inhibitor quinacrine and the cytochrome P450 inhibitor SKF525A, but were not inhibited by the cyclooxygenase inhibitor indomethacin. Quinacrine 110-120 phospholipase A2 group IB Rattus norvegicus 83-99 21658925-5 2011 Pretreatment with the PLA(2) inhibitor mepacrine (500 mug; i.c.v.) Quinacrine 39-48 phospholipase A2 group IB Rattus norvegicus 22-28 17628524-9 2007 However, mepacrine (PLA2 inhibitor) (1.1 and 2.2 micromol/animal, i.c.v.) Quinacrine 9-18 phospholipase A2 group IB Rattus norvegicus 20-24 18592376-2 2009 Assessed with propidium iodide and lactate dehydrogenase (LDH) leakage, neurodamage from ethanol (6 days 100 mM ethanol with four withdrawal periods) was prevented by the PLA2 pan-inhibitor, mepacrine. Quinacrine 191-200 phospholipase A2 group IB Rattus norvegicus 171-175