Biomedical subjects

F N Ko

Publications and source records attributed to F N Ko.

At least 37 records · Page 2Linked to original sources

PubMed1997

Bakkenolide G, a natural PAF-receptor antagonist.

Because platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) participates in many physiopathological responses, including inflammatory reaction, endotoxic shock, allergic diseases and platelet aggregation, PAF-receptor antagonists are important in the treatment of these diseases. A biologically active compound, bakkenolide G, extracted from the plant Petasites formosanus selectively and concentration-dependently inhibited PAF-induced platelet aggregation and ATP release. The IC50 of bakkenolide G for PAF (2 ng mL(-1))-induced platelet aggregation was 5.6 +/- 0.9 microM. Bakkenolide G also concentration-dependently inhibited PAF-induced intracellular signal transductions, including thromboxane B2 formation, and increased intra-cellular calcium concentration and phosphoinositide breakdown without affecting those caused by thrombin (0.1 units mL(-1)), collagen (10 microg mL(-1)), arachidonic acid (100 microM) and U46619 (1 microM). Bakkenolide G shifted the concentration-response curves of PAF-induced platelet aggregation parallel to the right; the Schild plot slope and the pA2 value were 1.31 +/- 0.31 and 6.21 +/- 0.75, respectively. Moreover, bakkenolide G concentration-dependently competed with [3H]PAF binding to platelets, with an IC50 value of 2.5 +/- 0.4 microM. These data strongly indicate that bakkenolide G is a specific PAF-receptor antagonist as an antiplatelet aggregatory agent.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1997

Antiplatelet effects of some aporphine and phenanthrene alkaloids in rabbits and man.

Two aporphines (boldine and laurolitsine) and five phenanthrene alkaloids (litebamine, secoboldine, N-cyanosecoboldine, N-methylsecoglaucine and N-methylsecopredicentrine) were evaluated in-vitro for their ability to inhibit platelet aggregation. All seven alkaloids inhibited aggregation of rabbit platelets and inhibited the release of ATP induced by arachidonic acid and collagen in rabbit platelets. Those aggregations induced by platelet-activating factor (PAF), thrombin, U46619 and ADP were inhibited by the three N-substituted secoboldine derivatives only. Thromboxane B2 formation caused by arachidonic acid was also suppressed by these compounds. They did not affect the generation of [3H]inositol monophosphate caused by collagen, PAF and thrombin in the presence of indomethacin. Platelet cyclic AMP level was unaffected by litebamine, but was increased by N-methylsecoglaucine. Litebamine suppressed the secondary aggregation, but not the primary aggregation, induced by ADP and adrenaline in platelet-rich plasma from man, whereas N-methylsecoglaucine inhibited both primary and secondary aggregation. It is concluded that the antiplatelet effect of these seven aporphine and phenanthrene alkaloids is mainly a result of inhibition of thromboxane A2 formation; N-methylsecoglaucine has additional antiplatelet activity as a result of increasing the levels of platelet cyclic AMP.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1997

2',5'-Dihydroxychalcone as a potent chemical mediator and cyclooxygenase inhibitor.

Eleven chalcone derivatives have been tested for their inhibitory effects on platelet aggregation in rabbit platelet suspension and the activation of mast cells and neutrophils. Arachidonic acid-induced platelet aggregation was potently inhibited by almost all the compounds and some also had a potent inhibitory effect on collagen-induced platelet aggregation and cyclooxygenase. Some hydroxychalcone derivatives showed strong inhibitory effects on the release of beta-glucuronidase and lysozyme, and on superoxide formation by rat neutrophils stimulated with the peptide fMet-Leu-Phe (fMLP). We found that the anti-inflammatory effect of 2',5'-dihydroxychalcone was greater than that of trifluoperazine. 2'5'-Dihydroxy and 2',3,4,5'-tetrahydroxyl chalcones, even at low concentration (50 microM), tested in platelet-rich plasma from man almost completely inhibited secondary aggregation induced by adrenaline. These results suggest that the anti-platelet effects of the chalcones are mainly a result of inhibition of thromboxane formation.

Animals↗

PubMed1997

Low-affinity thromboxane receptor mediates proliferation in cultured vascular smooth muscle cells of rats.

We examined the binding properties and mitogenic effects of U46619, using cultured vascular smooth muscle cells (VSMCs), by ligand-binding assay, measuring [3H]thymidine and [3H]leucine incorporation, checking with flow cytometry, and counting the cell number. The U46619-activated mitogenic signal-transduction pathway was assessed by measuring formation of inositol monophosphate (IP); [Ca2+]i; mitogen-activated protein kinase (MAPK), MAPK kinase (MAPKK), and p74raf-1 activities; and GTP-bound Ras. [3H]U46619 bound to cultured VSMCs from Wistar-Kyoto (WKY) rats at a single class of site (Kd: 15.5 +/- 2.6 nmol/L). However, it bound to VSMCs from spontaneously hypertensive rats (SHRs) at two classes of sites (Kd: 2.3 +/- 0.6 nmol/L and 1.4 +/- 0.5 mumol/L). U46619 increased DNA and protein synthesis, cell number, IP formation, [Ca2+]i, and MAPK and MAPKK activities, with EC50 values close to its Kd value for the low-affinity binding site in VSMCs from SHR. Prostaglandin (PG) E2 and PGF2 alpha showed little of such mitogenic effects. All these effects of U46619 were inhibited by SQ29548, staurosporine, or pretreatment of VSMCs with phorbol 12-myristate 13-acetate for 24 hours. However, U46619 stimulation did not lead to a significant increase in the Ras-GTP complex or p74raf-1 activity. In conclusion, the mitogenic effect of U46619 appears to be mediated via the activation of low-affinity thromboxane binding sites that trigger phosphoinositide hydrolysis and activate the MAPK pathway, leading to DNA synthesis and cell proliferation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1997

Pharmacological evaluation of ocoteine, isolated from Cassytha filiformis, as an alpha 1-adrenoceptor antagonist in rat thoracic aorta.

Ocoteine, isolated from Cassytha filiformis, was found to be an alpha 1-adrenoceptor blocking agent in rat thoracic aorta as revealed by its competitive antagonism of phenylephrine-induced vasoconstriction (pA2 = 7.67 +/- 0.09). Removal of endothelium from the aorta did not affect its antagonistic potency (pA2 = 7.97 +/- 0.07). [3H]-Inositol monophosphate formation caused by noradrenaline (3 microM) was suppressed by ocoteine (10 microM) and prazosin (3 microM). Ocoteine did not affect the contraction induced by U-46619, prostaglandin F2 alpha or angiotensin II, but inhibited slightly those by high K+ and endothelin I. Neither the cyclic AMP nor cyclic GMP content of rat thoracic aorta was changed by ocoteine (10 microM). Comparing the EC50 values, the potency of ocoteine against 5-hydroxytryptamine (5-HT) was about 60 times less than that against phenylephrine. Ocoteine (10 microM) also slightly antagonized the clonidine-induced inhibition of the twitch response evoked by field stimulation in rat vas deferens. In guinea pig trachea, the contraction caused by carbachol, histamine, neurokinin A or leukotriene C4 and beta 2-adrenoceptor-mediated relaxing responses induced by isoprenaline were not affected by ocoteine (10 microM). The voltage clamp study in rat ventricular single myocytes revealed that ocoteine (3, 10 microM) inhibited steady state outward currents, but not transient outward currents or slow inward Ca2+ currents. It is concluded that ocoteine is a selective alpha 1-adrenoceptor antagonist in isolated rat thoracic aorta. At high concentrations, it also blocks 5-HT receptors and Na+ and steady state outward currents in rat ventricular myocytes.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1997

ADP-mimicking platelet aggregation caused by rugosin E, an ellagitannin isolated from Rosa rugosa Thunb.

Among the nine ellagitannins, rugosin E was the most potent platelet aggregating agent with an EC50 of 1.5 +/- 0.1 microM in rabbit platelets and 3.2 +/- 0.1 microM in human platelets. The aggregations caused by rugosin E and ADP were inhibited by EGTA, PGE1, mepacrine, sodium nitroprusside and neomycin, but not by indomethacin, verapamil, TMB-8, BN52021 and GR32191B. Rugosin E-induced thromboxane formation was suppressed by indomethacin, EGTA, PGE1, verapamil, mepacrine, TMB-8 and neomycin. ADP-scavenging agents, such as CP/CPK and apyrase inhibited concentration-dependently ADP (20 microM)-, but not rugosin E (5 microM)-induced platelet aggregation. In thrombin (0.1 U/ml)-treated and degranulated platelets, rugosin E and ADP still caused 63.5 +/- 3.0% and 61.2 +/- 3.5% of platelet aggregation, respectively. Selective ADP receptor antagonists, ATP and FSBA inhibited rugosin E- and ADP-induced platelet aggregations in a concentration-dependent manner. Both rugosin E and ADP did not induce platelet aggregation in ADP (1 mM)-desensitized platelets. In contrast to ADP, rugosin E did not decrease cAMP formation in washed rabbit platelets. Both rugosin E and ADP did not cause phosphoinositide breakdown in [3H]myo-inositol-labeled rabbit platelets. In fura-2/AM-load platelets, both rugosin E and ADP induced increase in intracellular calcium concentration and these responses were inhibited by ATP and PGE1. All these data suggest that rugosin E may be an ADP receptor agonist in rabbit platelets.

Adenosine↗

PubMed1996

Antioxidant properties of isotorachrysone isolated from Rhamnus nakaharai.

Isotorachrysone inhibited iron-induced lipid peroxidation with an IC50 value of 1.64 +/- 0.08 microM in rat brain homogenates, and was comparable in potency to butylated hydroxytoluene and was more potent than alpha-tocopherol or desferrioxamine. The mechanism of antioxidant properties were then examined. Isotorachrysone could scavenge the stable free radical diphenyl-p-picrylhydrazyl. And it was an efficient direct scavenger of water-soluble peroxyl radicals with stoichiometry factor of 0.53 +/- 0.05 in the aqueous phase and also toward lipid-soluble peroxyl radicals in tissue homogenates. The oxygen consumption during peroxidation induced by radicals on human erythrocyte ghosts was suppressed by isotorachrysone. Furthermore, it was reactive towards superoxide anion with a second-order rate constant of 5.06 +/- 0.65 x 10(5) M-1 S-1. But it did not react with hydrogen peroxide detected within the sensitivity limit of our assay. Using ascorbate/iron ion/H2O2 as a hydroxyl radical generating system and deoxyribose as a probe, isotorachrysone was effective with hydroxyl radicals with a second-order rate constant of 3.88 +/- 0.54 x 10(11) M-1 S-1 under stimulation by iron-EDTA. On the other hand, isotorachrysone retarded the peroxidation of human low density lipoprotein (LDL) initiated by both aqueous and lipophilic peroxyl radicals. And it also suppressed copper-catalyzed human LDL oxidation, as measured by fluorescence intensity, electrophoretic mobility, and thiobarbituric acid-reactive substances formation in a concentration-dependent manner. Our results show that isotorachrysone is potentially an effective and versatile antioxidant, and can help protecting LDL against oxidation.

Animals↗

PubMed1996

Marchantin H as a natural antioxidant and free radical scavenger.

The antioxidant activity of marchantin H was investigated using various experimental models. Marchantin H inhibited nonenzymatic iron-induced lipid peroxidation in rat brain homogenates with an IC50 value of 0.51 +/- 0.03 microM. It was more potent than desferrioxamine or other classical antioxidants. Marchantin H also suppressed NADPH-dependent microsomal lipid peroxidation with an IC50 value of 0.32 +/- 0.01 microM without affecting microsomal electron transport of NADPH-cytochrome P450 reductase. Marchantin H could scavenge the stable free radical 1,1-diphenyl-2-picrylhydrazyl and peroxyl radical derived from 2,2 '-azobis(2-amidinopropane) dihydrochloride in aqueous phase, but not the peroxyl radical derived from 2,2 '-azobis(2,4-dimethylvaleronitrile) in hexane. The oxygen consumption during peroxyl radical-induced human erythrocyte ghost oxidation was decreased in a concentration-dependent manner by marchantin H. Furthermore, it was reactive toward superoxide anion generated by the xanthine/xanthine oxidase system. On the other hand, marchantin H inhibited copper-catalyzed oxidation of human low-density lipoprotein, as measured by fluorescence intensity, thiobarbituric acid-reactive substance formation, and electrophoretic mobility in a concentration-dependent manner. Our results indicate that marchantin H is a potentially effective and versatile antioxidant and can be used as a chaperone protecting biomacromolecules against peroxidative damage.

Animals↗

PubMed1996

Coagulation factor Xa stimulates platelet-derived growth factor release and mitogenesis in cultured vascular smooth muscle cells of rat.

The mitogenic effect of activated coagulation factor X (factor Xa) was examined in cultured aortic smooth muscle cells (VSMC) from Wistar-Kyoto rats (WKY). Factor Xa stimulated DNA synthesis and cell growth in VSMC, not through the phospholipase C-protein kinase C pathway because increase of inositol monophosphate (IP) accumulation and intracellular Ca2+ concentration was not observed, but probably via the PDGF receptor tyrosine kinase pathway since the pathway's components, Ras, Raf-1, MAPK (both 42 and 44 kD), and the transcription factors, c-Fos and c-Jun, were activated. These appeared to be effected by the serine protease activity of factor Xa, since in the presence of serine protease inhibitors such as PMSF, leupeptin, benzamidine, TAP anticoagulant, and TLCK, the latter three being specific inhibitors of the factor Xa, active site, the effects were completely blocked. Anti-factor Xa mAb, 5224, which specifically negated the activity of factor Xa, also inhibited completely the mitogenic effect of factor Xa, but not that of thrombin. Addition of PDGF did not affect the effect of factor Xa, which, however, was inhibited by anti-PDGF-AB antibody. This observation and the activation of PDGF receptor tyrosine kinase pathway suggested that the factor Xa might exert its effect via PDGF-like function. Direct measurement confirmed that factor Xa stimulated the release of PDGF from VSMC. Factor Xa, therefore, exerts serine protease activity on VSMC, causing somehow the release of PDGF, that in turn acts on the PDGF receptor tyrosine kinase; the pathway is then turned on, leading eventually to DNA synthesis and cell proliferation.

Animals↗

PubMed1996

Mechanism of catecholamine-induced proliferation of vascular smooth muscle cells.

BACKGROUND: Catecholamines have been shown to aggravate atherosclerosis in animals and humans, and abnormal proliferation of vascular smooth muscle cells (VSMC) is a key event in the early stage of atherosclerosis. Catecholamines may be involved in such cell growth. Therefore, a series of experiments using cultured VSMC was performed to elucidate their possible mitogenic effect. METHODS AND RESULTS: We examined the mitogenic effect of catecholamines using rat aortic smooth muscle cells (VSMC) by measuring [3H]thymidine incorporation, checking with flow cytometry, and counting the cell number directly. Furthermore, the catecholamine-activated signal transduction pathway was assessed by measurement of the formation of inositol 1, 4, 5-triphosphate, intracellular Ca2+ concentration, mitogen-activated protein kinase (MAPK) activity, and mitogenic gene expression. Norepinephrine (NE) and phenylephrine stimulated [3H]thymidine incorporation and cell growth. Clonidine and isoproterenol showed little of such effects. Prazosin was more effective than either yohimbine or propranolol in suppressing the mitogenic effect of NE, indicating that catecholamine-induced VSMC proliferation is mediated by alpha 1-adrenoceptors. The alpha 1-adrenoceptor activation was coupled to pertussis toxin-insensitive Gq-protein and triggered phosphoinositide hydrolysis with subsequent activation of protein kinase C and MAPK in VSMC. In response to NE, both 42- and 44-kD MAPK were activated and tyrosine was phosphorylated. alpha 1-Adrenoceptor stimulation with NE also caused accumulation of c-fos, c-jun, and c-myc mRNA. Chloroethylclonidine completely blocked the alpha 1-adrenoceptor-mediated mitogenesis. CONCLUSIONS: The effect of catecholamines appears to be mediated via the activation of the chloroethylclonidine-sensitive alpha 1-adrenoceptors that triggers the phosphoinositide hydrolysis and activates the MAPK pathway, leading to DNA synthesis and cell proliferation.

Animals↗

PubMed1996

Inhibition by tamsulosin of tension responses of human hyperplastic prostate to electrical field stimulation.

Tamsulosin (10(-10)-10(-9) M) or prazosin (10(-9)-10(-8) M) concentration dependently blocked the tension responses to electrical field stimulation (0.3 ms duration, 80 V and 20 Hz) in human hyperplastic prostate with lC50 values of (1.93 +/- 0.26) x 10(-10) M and (2.11 +/- 0.21) x 10(-9) M, respectively. The relative potency of tamsulosin with reference to prazosin was 10.96. The pA2 values for tamsulosin and prazosin against phenylephrine-induced contractions were 10.05 +/- 0.16 and 9.25 +/- 0.07, respectively. The relative potency of tamsulosin with reference to prazosin was 6.31. In the presence of prazosin to block alpha 1-adrenoceptor-mediated responses, nifedipine (10(-5) M), but not tamsulosin (10(-9) M), significantly blocked the tension responses in human hyperplastic prostate induced by increasing [Ca2+]o concentrations (10(-4) to 3 x 10(-3) M) in a Ca(2+)-free environment pre-depolarized with 60 mM K+. Additionally, the effects of prazosin and tamsulosin on electrical field stimulation-evoked [3H]noradrenaline release were studied on the S3/S2 ratios. It appeared that both drugs had little effect on this release reaction, with S3/S2 ratios of 0.96 +/- 0.02 and 0.90 +/- 0.02, respectively. These results indicate that tamsulosin is a potent antagonist against endogenous sympathetic stimulation in human hyperplastic prostate.

Adrenergic alpha-Agonists↗

PubMed1996

N-allylsecoboldine as a novel antioxidant against peroxidative damage.

N-Allylsecoboldine was evaluated for antioxidant properties by studying its ability to react with relevant reactive oxygen species, and its protective effect on human erythrocytes under oxidative stress. Using brain homogenates, we found that N-allylsecoboldine dose dependently inhibited lipid peroxidation (IC50 = 4.80 +/- 0.16 microM) and markedly scavenged stable nitrogen-centered radicals. N-Allylsecoboldine was a very efficient scavenger for inhibiting peroxyl radical-mediated destruction of B-phycoerythrin, with a stoichiometry factor of 4.40 +/- 0.59. It also trapped the hydroxyl radicals with a second-order rate constant of 6.92 +/- 0.86 x 10(9) M-1 S-1. Additionally, human erythrocyte oxidative hemolysis induced by aqueous peroxyl radical or hydrogen peroxide was suppressed by N-allylsecoboldine. It not only attenuated the extent of lipid peroxidation but also decreased the formation of the high-molecular weight proteins and degradation of the band 6 protein in radical-treated erythrocytes. It also inhibited the shortening of Russell's viper venom-clotting time mediated by prelytic radical-treated erythrocytes. In the presence of exogenous oxidative stress, hemolysis and lipid peroxidation were significantly enhanced in beta-thalassemic erythrocytes, as compared to the normal control. These elevated detrimental effects could be prevented by N-allylsecoboldine. It is concluded that N-allylsecoboldine may act as an effective antioxidant and protect cells against oxidative damage.

Amidines↗

PubMed1996

Mechanisms-regulated platelet spreading after initial platelet contact with collagen.

In static condition, 6F1, an anti-glycoprotein Ia/IIa monoclonal antibody, almost completely prevented initial platelet adhesion to fibrillar collagen, but markedly lost its action with prolonged incubation. The platelet adhesion and spreading at the later stage were prevented by adding the peptide GRGDS, aspirin, and apyrase, suggesting that after initial recognition of platelet glycoprotein Ia/IIa with collagen the activation of glycoprotein IIb/IIIa and the release of thromboxane A2/ADP would promote platelet spreading, thus strengthening the stability of adhesion. Both initial platelet adhesion and platelet spreading were prevented by cytochalasin B, an inhibitor of actin polymerization. In contrast, BAPTA (an intracellular Ca2+ chelator) only inhibited platelet spreading. Inhibition of protein kinase C or protein tyrosine kinase by staurosporine or genistein, respectively, had only little effect on platelet adhesion. These data suggest that actin polymerization and intracellular Ca2+ mobilization are involved in the regulation of platelet spreading after initial platelet contact with collagen.

Animals↗

PubMed1996

Antiproliferative effect in rat vascular smooth muscle cells by osthole, isolated from Angelica pubescens.

The antiproliferative effect of osthole on rat vascular smooth muscle cells was examined in this study. A number of mitogenic agents, e.g., foetal-calf serum (10%, v/v) and platelet-derived growth factor (20 ng/ml), and pharmacological agents, e.g., serotonin (10 microM), ionomycin (3 nM), phorbol 12,13-dibutyrate (20 nM) and phorbol myristate acetate (200 nM), were used to induce DNA synthesis in rat vascular smooth muscle cells; these effects were concentration dependently inhibited by osthole and the half-maximal inhibition (IC50) occurred at 13.6 +/- 1.8, 11.8 +/- 1.3, 7.9 +/- 0.9, 7.1 +/- 0.2, 7.8 +/- 0.2 and 8.6 +/- 0.4 microM, respectively. Osthole itself increased the cyclic AMP and cyclic GMP formations in a concentration-dependent manner; it synergistically increase cyclic AMP and cyclic GMP levels induced by forskolin and sodium nitroprusside, respectively. After 48 h deprivation of serum, cells were re-stimulated with serum and the cell cycle was observed by flow cytometry; treatment of cells with osthole (100 microM) caused a block of serum-inducible cell cycle progression at a point before the G1-S boundary. The addition of osthole (100 microM) at various times after serum addition to serum-deprived cells showed full inhibition of DNA synthesis even when added 6 h after serum. The cell cycle progression block was gradually lost as the delay from serum to osthole application was increased from 6 to 18 h. The effect of osthole on serum-stimulated [3H]thymidine incorporation into endothelial cells was examined and the IC50 value (158.7 +/- 2.7 microM, n = 6) was obtained; it exhibited greater potency (12-fold) for vascular smooth muscle cells as compared with endothelial cells as an antiproliferative agent. These results suggest that osthole is a selective antiproliferative agent in vascular smooth muscle cells. The antiproliferative effect occurs at the early G1 phase of the cell cycle and is due to the increase in cyclic AMP and cyclic GMP contents.

Animals↗

PubMed1996

Coumarins and antiplatelet aggregation constituents from Formosan Peucedanum japonicum.

Four new khellactone esters, (-)-trans-3'-acetyl-4'-senecioylkhellactone, (+-)-cis-3'-acetyl-4'-tigloylkhellactone, (+-)-cis-4-tigloylkhellactone, (+)-trans-4'-tigloylkhellactone, together with 14 known coumarins, isoimperatorin, psoralen, bergapten, xanthotoxol, cnidilin, (-)-selinidin, (-)-deltoin, (+)-pteryxin, (+)-peucedanocoumarin III, xanthotoxin, imperatorin, (+)-marmesin, (+)-oxypeucedanin hydrate, (+)-peucedanol and three chromones, eugenin, (-)-hamaudol, (+)-visamminol, have been isolated from the root of Formosan Peucedanum japonicum. The structures of the new compounds were elucidated by spectral data. The identities of (+)-trans-3'-tigloyl-4'-acetylkhellactone, formerly reported as a new compound, and (+)-cis-3'-angeloyl-4'-acetyl-khellactone, with the known (+)-peucedanocoumarin III and (+)-pteryxin, respectively, are discussed. Among the isolates, seven compounds, eugenin, (-)-selinidin, (+)-pteryxin, imperatorin, bergapten, cnidilin and (+)-visamminol, show strong antiplatelet aggregation activity in vitro.

Coumarins↗

PubMed1996

Antiplatelet of vasorelaxing actions of some benzylisoquinoline and phenanthrene alkaloids.

Members of a series of benzylisoquinoline and phenanthrene alkaloids were tested for their antiplatelet and vasorelaxing actions. Atherosperminine HClO4 (15) and atherosperminium I (16) showed strong inhibition of adenosine 5'-diphosphate-induced platelet aggregation. dl-N-Methylcoclaurine (1), dl-coclaurine (6), 15, 16, xylopine hydroxylamine (18), and atherosperminine N-oxide (19) showed strong inhibition of arachidonic acid-induced platelet aggregation. Compounds 1, 15, 16, dicentrine methine (17), 18, and 19 showed strong inhibition of collagen-induced platelet aggregation. d-(-)-Magnocurarine I (8), 15, and 16 showed strong inhibition of platelet-activating factor-induced platelet aggregation. Compounds 15, 17, and 19 showed vasorelaxing action in rat thoracic aorta.

Alkaloids↗

PubMed1996

Novel antiplatelet constituents from formosan moraceous plants.

Sixteen constituents from Formosan Moraceous plants were tested for their antiplatelet activities in rabbit platelet suspension and human platelet-rich plasma. Cycloartocarpin A, cycloheterophyllin, broussochalcone A, kazinol A, broussoaurone A, and broussoflavonol F showed strong inhibition of arachidonic acid (AA)-induced platelet aggregation. Of the compounds tested, broussochalcone A exhibited the most potent inhibition of platelet aggregation induced by AA (IC50 = 6.8 microM). The antiplatelet effects of cycloheterophyllin, broussochalcone A, kazinol B, broussoaurone A, and broussoflavonol F are partially due to an inhibitory effect on cyclooxygenase.

Animals↗

PubMed1996

Antiplatelet arylnaphthalide lignans from Justicia procumbens.

Fractionation of the EtOH extract of Justicia procumbens, guided by antiplatelet bioassay, led to the isolation of nine known arylnaphthalide lignans, neojusticin A (1), justicidin B (2), justicidin A (3), taiwanin E methyl ether (4), neojusticin B (5), chinensinaphthol methyl ether (6), taiwanin E (8), chinensinaphthol (9), and diphyllin (10), and a new arylnaphthalide lignan that was characterized by spectral means as 4'-demethylchinensinaphthol methyl ether (7). Compounds 1, 2, 4, and 8 significantly inhibited platelet aggregation.

Animals↗