Biomedical subjects

C M Teng

Publications and source records attributed to C M Teng.

At least 127 records · Page 7Linked to original sources

PubMed1995

Vasodilator agents modulate rat glomerular mesangial cell growth and collagen synthesis.

Mesangial cell activation and extracellular matrix accumulation are hallmarks of many forms of glomerulonephropathy. We investigated the effect of several agents possessing vasodilating activities on rat mesangial cell growth and collagen synthesis. Using cell counting and a modified MTT assay, it was shown that dipyridamole, pentoxifylline, dicentrine, prazosin and doxazosin all caused a dose-dependent inhibition of serum-stimulated rat mesangial cell proliferation. Platelet-derived growth factor-induced cell proliferation was also inhibited by doxazosin and pentoxifylline. Dipyridamole and pentoxifylline inhibited collagen synthesis in confluent mesangial cells while dicentrine and doxazosin did not. The procollagen alpha 1 (I) mRNA expression was also decreased by dipyridamole and pentoxifylline. These results suggested that, in addition to dipyridamole, pentoxifylline and alpha 1-adrenoceptor blockers may have a potential to delay the progression of chronic glomerulopathy associated with mesangial proliferation.

Analysis of Variance↗

PubMed1995

Effects of dicentrine on the mechanical properties of systemic arterial trees in dogs.

We evaluated the effects of dicentrine on the physical properties of systemic arterial trees. Dicentrine, isolated from Lindera megaphylla, was identified as a potent, selective alpha 1-adrenoceptor antagonist. We used high-fidelity multisensor catheter to measure the ascending aortic pressure and flow signals in 9 mongrel dogs. A succinct T-tube model with vascular nonuniformity was adopted to relate the pulsatile pressure and flow waves. The model-estimated parameters were capable of representing the mechanical properties of the blood vessel walls. Dicentrine had a beneficial effect on the rigidity of head and body circulation, respectively. There were great improvements not only in the tube distensibility and wave transmission time, but also in the peripheral load compliance and resistance. In global circulation that was defined as the parallel combination of head and body circulation, dicentrine significantly reduced values in characteristic impedance of the ascending aorta from 164 +/- 67 to 105 +/- 43 dynes/s/cm5, and in wave reflection factor from 0.46 +/- 0.14 to 0.36 +/- 0.13, and in total peripheral vascular resistance from 4,751 +/- 1,226 to 3,581 +/- 1,277 dynes/s/cm5. On the other hand, total peripheral load compliance was increased from 0.2950 +/- 0.1794 to 0.4457 +/- 0.2199 ml/mm Hg. Cardiac output (CO) and heart rate (HR) remained unchanged, however. Dicentrine had an impact on the mechanical properties of Windkessel vessels and resistance vessels in the systemic circulation.

Adrenergic alpha-Antagonists↗

PubMed1994

YC-1, a novel activator of platelet guanylate cyclase.

YC-1 [3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole] inhibited the aggregation of and ATP release from washed rabbit platelets induced by arachidonic acid (AA), collagen, U46619, platelet-activating factor (PAF), and thrombin in a concentration-dependent manner. YC-1 also disaggregated the clumped platelets caused by these inducers. The thromboxane B2 formation caused by collagen, PAF, and thrombin was inhibited by concentrations of YC-1 that did not affect formation of thromboxane B2 and prostaglandin D2 caused by AA. YC-1 suppressed the increase of intracellular Ca2+ concentration and generation of inositol 1,4,5-trisphosphate caused by these five aggregation inducers. Both the cAMP and cGMP contents of platelets were increased by YC-1 in a concentration- and time-dependent manner. Like sodium nitroprusside, YC-1 potentiated formation of cAMP caused by prostaglandin E1 but not that by 3-isobutyl-1-methylxanthine. Adenylate cyclase and cAMP phosphodiesterase activities were not altered by YC-1. Activity of cGMP phosphodiesterase was unaffected by YC-1. Activities of guanylate cyclase in platelet homogenate and cytosolic fraction were activated by YC-1, whereas particulate guanylate cyclase activity was unaffected. The antiplatelet effect of sodium nitroprusside but not that of YC-1 was blocked by hemoglobin and potentiated by superoxide dismutase. After intraperitoneal administration for 30 minutes, YC-1 prolonged the tail bleeding time of conscious mice. These data indicate that YC-1 is a direct soluble guanylate cyclase activator in rabbit platelets. It may also possess antithrombotic potential in vivo.

1-Methyl-3-isobutylxanthine↗

PubMed1994

Protracted treatment with phorbol ester modulates J-7 human hepatoma-cell-induced aggregation and coagulation of human platelet-rich plasma.

In heparinized human platelet-rich plasma (PRP), J-7 human hepatoma cells initially induced platelet aggregation; then a clot formed. ADP-scavenger systems, apyrase and creatine phosphate/creatine phosphokinase did not inhibit this tumor-cell-induced platelet aggregation (TCIPA), whereas hirudin and concanavalin A completely blocked it. J-7 cells also shortened the recalcification time of normal and of Factor-VIII- and IX-deficient human plasma, although it was inactive in shortening the recalcification time of Factor-VII-deficient plasma. After treatment with phorbol 12,13-dibutyrate (PDBu) for 5 to 90 min, the aggregation and coagulation abilities of J-7 cells were unaffected. Prolonged treatment of J-7 cells with PDBu but not with alpha-PDBu for 24 and 72 hr resulted in gradual loss of aggregation and coagulation. Staurosporine antagonized the effect of PDBu and restored aggregation and coagulation in J-7 cells. Protracted treatment with PDBu (24 or 72 hr) did not affect adherence of J-7 cells to the extracellular-matrix proteins (i.e., fibrinogen, fibronectin, laminin, vitronectin and collagen types I and IV) or to the surface of plastic culture dishes. The treatment also did not affect J-7 cell detachment from plastic culture dishes. These in vitro results demonstrate that protracted phorbol ester treatment diminishes TCIPA and blood coagulation of tumor cells.

Alkaloids↗

PubMed1994

Functional identification of alpha 1-adrenoceptor subtypes in human prostate: comparison with those in rat vas deferens and spleen.

The effects of some alpha 1-adrenoceptor antagonists (prazosin, nonselective for the alpha 1A- and alpha 1B-adrenoceptor subtypes; 5-methyl-urapidil, selective for the alpha 1A-adrenoceptor subtype; chloroethylclonidine, selective for the alpha 1B-adrenoceptor subtype) and nifedipine were compared on contractile responses to noradrenaline or phenylephrine in human prostatic tissues, rat vas deferens and spleen. In rat vas deferens, nifedipine (1 microM), but not chloroethylclonidine (100 microM), almost completely abolished noradrenaline-induced contraction, the pA2 values for prazosin and 5-methyl-urapidil against noradrenaline being 9.29 and 8.55, respectively. In rat spleen, chloroethylclonidine reduced (by 57%) the maximum contraction induced by phenylephrine; nifedipine was ineffective. The log concentration-response curve was shifted significantly to the right; the pA2 values of prazosin and 5-methyl-urapidil against phenylephrine were 9.45 and 7.21, respectively. In human prostatic tissues, both nifedipine and chloroethylclonidine produced significant inhibition of noradrenaline-induced contractions. Chloroethylclonidine produced a 44% reduction of the maximum contraction to noradrenaline and shifted the log concentration-response curve to the right. In contrast, nifedipine, while reducing the maximum response to a similar extent, produced a small rightward shift in the log concentration-response curve. The pA2 values for prazosin and 5-methyl-urapidil against noradrenaline were 9.21 and 7.74, respectively. The pA2 values for prazosin in these three tissues did not vary significantly, whereas that for 5-methyl-urapidil in human prostatic tissue was intermediate between that in rat vas deferens and that in rat spleen: these tissues contain primarily alpha 1A- and alpha 1B-adrenoceptor subtypes, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1994

Antiplatelet effects of clausine-D isolated from Clausena excavata.

Clausine-D inhibited concentration-dependently the aggregation and release reaction of washed rabbit platelets induced by arachidonic acid and collagen, without affecting those induced by U46619, PAF and thrombin. The IC50 values of clausine-D on arachidonic acid- and collagen-induced platelet aggregation were calculated to be 9.0 +/- 1.1 and 58.9 +/- 0.9 microM, respectively. Thromboxane B2 and prostaglandin D2 formation in platelets caused by arachidonic acid were also suppressed. Clausine-D inhibited increased intracellular concentration of calcium in platelets caused by arachidonic acid and collagen, and also abolished the generation of inositol monophosphate caused by arachidonic acid, but not that by collagen, U46619, PAF and thrombin. In human citrated platelet-rich plasma, clausine-D inhibited the secondary phase, but not the primary phase, of aggregation induced by epinephrine and ADP. These results indicate that the antiplatelet effect of clausine-D is due to inhibition of the formation of thromboxane A2.

Adenosine Diphosphate↗

PubMed1994

Inhibition of cyclooxygenase activity and increase in platelet cyclic AMP by girinimbine, isolated from Murraya euchrestifolia.

Girinimbine is an antiplatelet agent isolated from Murraya euchrestifolia. In washed rabbit platelets, it inhibited arachidonic acid (AA)-, collagen-, U46619- and platelet-activating factor (PAF)-induced aggregation and ATP release in a concentration-dependent manner with IC50 values of 9.1 +/- 1.5, 16.7 +/- 1.7, 60.0 +/- 5.1 and 71.9 +/- 5.6 microM, respectively. However, it did not apparently affect thrombin-induced aggregation and ATP release even when a concentration of 80 microM was used. In citrated human platelet-rich plasma (PRP), girinimbine selectively inhibited secondary aggregation and ATP release without appearing to affect the primary aggregation induced by epinephrine and ADP. The formation of both platelet thromboxane B2 (TxB2) and prostaglandin D2 (PGD2) caused by AA was inhibited by girinimbine concentration dependently, with a maximal effect at 20 microM. Girinimbine also inhibited cyclooxygenase activity as reflected by the attenuation of prostaglandin E2 (PGE2) formation after incubation of sheep vesicular gland microsomes with arachidonic acid. In myo-[3H]inositol-labeled and fura-2-loaded platelets, [3H]inositol monophosphate generation and the increase in intracellular Ca2+ ([Ca2+]i) stimulated by AA and collagen, but not that stimulated by U46619, PAF and thrombin, were inhibited by girinimbine (20 microM). Platelet cyclic AMP levels were elevated by high concentrations of girinimbine (20 and 80 microM). These data indicate that the antiplatelet effect of girinimbine is due to the inhibition of cyclooxygenase activity and elevation of the cyclic AMP level.

Adenosine Triphosphate↗

PubMed1994

The effect of 3-[2-(cyclopropylamino)ethoxy]xanthone on platelet thromboxane formation.

A synthetic xanthone derivative, 3-[2-(cyclopropylamino)ethoxy] xanthone (CPEX), was investigated for its antiplatelet activities in washed rabbit platelets and human platelet-rich plasma. CPEX inhibited concentration-dependently the aggregation and ATP release of rabbit platelets caused by arachidonic acid (AA; 100 microM) and collagen (10 micrograms/ml), but not those by thrombin (0.1 U/ml), PAF (2 ng/ml), and U46619 (1 microM). The IC50 value of CPEX on AA-induced aggregation was 10.9 +/- 2.1 microM (n = 7). Thromboxane B2 formations caused by AA, collagen, and thrombin were inhibited by CPEX (20 microM), and prostaglandin D2 formation caused by AA was also inhibited. In human platelet-rich plasma, CPEX specifically inhibited the secondary aggregation and the release reaction induced by epinephrine (5 microM) and ADP (3 microM). CPEX also inhibited AA- and collagen-induced inositol-phosphate formation in [3H]myo-inositol-labeled platelets and intracellular Ca2+ increase in fura-2/AM-loaded platelets, respectively, without affecting those induced by PAF, thrombin, and U46619 in the presence of indomethacin (5 microM). These data suggest that the antiplatelet effect of CPEX is due to an inhibitory effect on the cyclooxygenase and then leads to the decrease of thromboxane formation.

Adenosine Triphosphate↗

PubMed1994

Cinnamophilin, a novel thromboxane A2 receptor antagonist, isolated from Cinnamomum philippinense.

The pharmacological activity of cinnamophilin ((8R,8'S)-4,4'-dihydroxy-3,3'-dimethoxy-7-oxo-8,8'-neolignan), isolated from Cinnamomum philippinense, was studied in isolated rat aorta, guinea-pig trachea and rabbit platelets. Cinnamophilin was found to be a thromboxane A2 receptor blocking agent in these tissues as revealed by its competitive antagonism of the U-46619 (9,11-dideoxymethanoepoxy-9 alpha,11 alpha-prostaglandin F2 alpha)-induced contraction of rat aorta and guinea-pig trachea and aggregation of rabbit platelets with pA2 values of 7.3 +/- 0.2, 5.2 +/- 0.1 and 6.3 +/- 0.3, respectively. Protection against the irreversible vasoconstriction of rat aorta caused by U-46619 (0.05 microM) was obtained by cinnamophilin (10 microM) but not by caffeine (25 mM). Cinnamophilin (1-15 microM) also possessed voltage-dependent Ca2+ channel blocking action, judging from its antagonism of the high K+ (60 mM)- and Bay K 8644 (0.1 microM)-induced contraction in rat thoracic aorta. Cinnamophilin (30 microM) produced a slight relaxation of noradrenaline (3 microM)-induced tonic contractions, and this relaxing effect was abolished in the presence of nifedipine (1 microM). Nifedipine (10 microM) sufficient to inhibit high K(+)-induced contractions failed to attenuate the contractile response to U-46619. A high concentration of cinnamophilin (100 microM) did not affect the aortic contraction induced by endothelin-1, angiotensin II, carbachol or serotonin. Neither cAMP nor cGMP in rat aorta was increased by cinnamophilin. These results indicate that cinnamophilin is a selective thromboxane A2 receptor antagonist especially in rat aorta, and also possesses voltage-dependent Ca2+ channel blocking properties.

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

PubMed1994

Magnolol and honokiol isolated from Magnolia officinalis protect rat heart mitochondria against lipid peroxidation.

In isolated rat heart mitochondria lipid peroxidation was induced with ADP and ferrous sulfate (FeSO4). Oxygen consumption and malondialdehyde (MDA) production were measured to quantitate lipid peroxidation. The antioxidant effects of magnolol and honokiol purified from Magnolia officinalis were 1000 times higher than that of alpha-tocopherol. The IC50 values of magnolol and honokiol for inhibition of oxygen consumption were 8.0 x 10(-8) M and 1.0 x 10(-7) M, respectively, while that of alpha-tocopherol was 1.0 x 10(-4) M. Magnolol at 0.5 microM inhibited 71.4 +/- 9.4% of oxygen consumption and 59.3 +/- 4.6% MDA production. At the same concentration, honokiol inhibited 78.1 +/- 4.7% of oxygen consumption and 86.9 +/- 4.0% of MDA production. Of conjugated diene formation 48.4 +/- 4.6% and 53.1 +/- 3.4% were inhibited by 0.5 microM magnolol and honokiol, respectively. Also both magnolol and honokiol exhibited free radical scavenging activities as shown by the diphenyl-p-picrylhydrazyl assay, but they were less potent than alpha-tocopherol.

Animals↗

PubMed1994

Effects of dicentrine, a novel alpha 1-adrenoceptor antagonist, on human hyperplastic prostates.

The effects of dicentrine, an alpha 1-adrenoceptor antagonist, on human hyperplastic prostates were investigated by radioligand binding and in vitro isometric tension experiments. In human hyperplastic prostates, alpha 1-adrenoceptors were characterized by a binding assay using [3H]prazosin as a radioligand. Specific [3H]prazosin binding was saturable and of high affinity (Kd = 0.2 +/- 0.02 nM) with a maximal number of binding sites (Bmax = 55.2 +/- 3.2 fmol/mg protein). alpha-Adrenoceptor antagonists competed with [3H]prazosin for binding in the order: dicentrine > phentolamine > rauwolscine. Norepinephrine (0.3-100 microM) or phenylephrine (1-300 microM) produced gradual contractions of human hyperplastic prostates. The concentration-response curve of norepinephrine or phenylephrine was shifted in parallel to the right by dicentrine, consistent with a competitive blockade. The pA2 values of dicentrine against norepinephrine and phenylephrine were 8.04 +/- 0.09 and 8.33 +/- 0.11, respectively. These experiments were conducted to confirm that there was no interaction between alpha 1- and alpha 2-adrenoceptors in the tissue. Rauwolscine (1 microM) caused 1.7-fold, while dicentrine (0.1 microM) caused 15.8-fold shift of norepinephrine-induced contraction of human hyperplastic prostates. Combination of rauwolscine with dicentrine caused 17.8-fold shift of norepinephrine-induced prostatic tissue contraction. The contractile response to transmural field stimulation was abolished by pretreatment with tetrodotoxin, and suppressed concentration dependently by dicentrine or prazosin, whereas rauwolscine had little effect. It is concluded that dicentrine inhibits human hyperplastic prostate contractions in response to exogenous and endogenous adrenergic stimulation. Dicentrine may thus hold potential to relieve bladder outlet obstruction caused by benign prostatic hyperplasia via alpha 1-adrenoceptor blockade.

Adrenergic alpha-Antagonists↗

PubMed1994

Inhibitory effect of norathyriol, a xanthone from Tripterospermum lanceolatum, on cutaneous plasma extravasation.

Norathyriol, a xanthone aglycon isolated from Tripterospermum lanceolatum, was demonstrated to reduce the plasma leakage elicited by the passive cutaneous anaphylactic reaction in normal as well as in adrenalectomized mice. Capsaicin pretreatment greatly suppressed the local edema caused by antidromic stimulation of the saphenous nerve. The plasma exudation of neurogenic inflammation was also reduced in mice treated with norathyriol, diphenhydramine and methysergide, but not with indomethacin. Norathyriol, cyproheptadine and diphenhydramine combined with methysergide suppressed the ear edema caused by injection of compound 48/80, bradykinin and substance P into the ear. However, indomethacin did not affect this phlogist-induced edema response. Histamine- and serotonin-induced plasma exudation in ear edema was also reduced by norathyriol. In isolated rat peritoneal mast cell preparations, norathyriol produced a dose-dependent inhibition of histamine and beta-glucuronidase release from mast cells challenged by compound 48/80, bradykinin and substance P. In compound 48/80-pretreated mice, norathyriol at higher concentrations suppressed the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine combined with methysergide did. These data indicate that the inhibitory effect of norathyriol on local edema is not due to the release of steroid hormones from the adrenal gland, but is probably partly due to suppression of mast cell degranulation and hence reduce the release of chemical mediators which increase vascular permeability, and partly, at least in higher doses, due to protection of the vasculature from challenge by various mediators.

Adrenalectomy↗

PubMed1994

gamma-Pyrone compounds. 5. Synthesis and antiplatelet effects of xanthonoxypropanolamines and related compounds.

A series of simple xanthonoxypropanolamines and related compounds were synthesized. 3-[3-(Cyclopropylamino)propoxy]-xanthone showed same potent antiplatelet effects as norathyriol tetraacetate on arachidonate-induced aggregation. 3-[3-(Cyclohexylamino)-2-hydroxypropoxy]xanthone showed more potent antiplatelet effects than norathyriol tetraacetate on collagen-induced aggregation. The various amino groups of the oxypropanolamine or oxypropylamine side chains of the synthesized compounds regulated the antiplatelet effects.

Animals↗

PubMed1994

The relaxant action of osthole isolated from Angelica pubescens in guinea-pig trachea.

The effect of osthole, isolated from Angelica pubescens, on the contraction of guinea-pig trachea was studied. Osthole (25-100 mumol/l), theophylline (10-1000 mumol/l) and higher concentrations of nifedipine (0.1-100 mumol/l) suppressed the contraction response curves of tracheal smooth muscle caused by carbachol, prostaglandin F2 alpha (PGF2 alpha), U46619 (thromboxane A2 analogue) and leukotriene C4 (LTC4) in a concentration-dependent manner. The contraction caused by high K+ (120 mmol/l) and cumulative concentrations of CaCl2 (0.03-3 mmol/l) was also inhibited concentration-dependently by osthole (25-100 mumol/l), theophylline (10-1000 mumol/l) and lower concentrations of nifedipine (0.01-0.1 mumol/l). The relaxant actions of osthole were not affected by propranolol (1 mumol/l), glibenclamide (10 mumol/l) or removal of tracheal epithelium. Osthole (100 mumol/l) was still effective in causing tracheal relaxation in the presence of nifedipine (1 mumol/l). In Ca(2+)-free- and EGTA (0.2 mmol/l)-containing medium, the relaxing effect of osthole was more potent than in normal Krebs solution. Osthole (25 and 50 mumol/l) caused 2.9 and 6.5, or 3.0 and 5.6 fold, respectively, increase in potency of forskolin or sodium nitroprusside in causing tracheal relaxation but did not affect that by cromakalim. Osthole (50 mumol/l) enhanced the increase in tissue cAMP and cGMP levels induced by forskolin and sodium nitroprusside, respectively, and in higher concentrations (100 and 250 mumol/l), itself increased markedly tissue cAMP and cGMP contents. Osthole (10-250 mol/l) inhibited the activity of cAMP and cGMP phosphodiesterases in a concentration-dependent manner. It is concluded that osthole exerts a non-specific relaxant effect on the trachealis by inhibiting the cAMP and cGMP phosphodiesterases.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1994

Effect of norathyriol, isolated from Tripterospermum lanceolatum, on A23187-induced pleurisy and analgesia in mice.

A23187-induced pleurisy in the mouse was demonstrated in this study. The protein leakage, leukocyte accumulation, LTB4 and PGE2 production in the pleural cavity of mice were increased by A23187 in a dose-dependent manner. At 7.5 nmole A23187 intrapleural injection, the protein level peaked at 0.5-2 h, PMN leukocytes accumulation peaked at 3-4 h, and LTB4 and PGE2 production peaked at 0.5-1 h. In this in vivo model we investigated the anti-inflammatory effect of norathyriol, isolated from Tripterospermum lanceolatum. A23187-induced protein leakage was reduced by norathyriol (ID50 was about 30.6 mg/kg i.p.), indomethacin and BW755C. A23187-induced PMN leukocytes accumulation was suppressed by norathyriol (ID50 was about 16.8 mg/kg, i.p.) and BW755C, while enhanced by indomethacin. Like BW755C, norathyriol reduced both LTB4 and PGE2 production (ID50 was about 18.6 and 29.1 mg/kg i.p., respectively), while indomethacin reduced PGE2 but not LTB4 generation. We also demonstrated the analgesic effect of norathyriol on the acetic acid-induced writhing response. Acetic acid-induced writhing response was depressed by norathyriol (ID50 was about 27.9 mg/kg i.p.), indomethacin and ibuprofen. These results suggest that norathyriol, like BW755C, might be a dual, yet weak, cyclooxygenase and lipoxygenase pathway blocker. The inhibitory effect of norathyriol on the A23187-induced pleurisy and acetic acid-induced writhing response in mice is proposed to be dependent on the reduction of eicosanoids mediators formation in the inflammatory site.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

PubMed1994

Mechanisms of vasorelaxation induced by N-allylsecoboldine in rat thoracic aorta.

N-Allylsecoboldine was shown to be the most effective of several boldine derivatives that were tested for their vasorelaxing effect on the rat aorta. In KCl (60 mmol/l) medium, Ca2+ (0.03-3 mmol/l)-induced vasoconstriction was inhibited, concentration-dependently, by N-allylsecoboldine. The IC50 for N-allylsecoboldine was calculated to be about 4 mumol/l (for a Ca2+ concentration of 1 mmol/l). The vasorelaxant effect on KCl-induced responses was more pronounced at 60 mmol/l KCl than at 15 mmol/l KCl. Contraction of rat aorta in response to phenylephrine (0.01-100 mumol/l) was concentration-dependently inhibited by N-allylsecoboldine and by verapamil (3-30 mumol/l), while contraction in response to B-HT 920, serotonin or PGF2 alpha was not affected. This relaxing effect of N-allylsecoboldine persisted in endothelium-denuded aorta. In cultured A10 vascular smooth muscle cells, N-allylsecoboldine and verapamil displaced the binding of [3H]-prazosin (Ki values = 0.4 +/- 0.2 and 0.6 +/- 0.2 mumol/l, respectively). The increase of inositol monophosphate caused by phenylephrine in rat aorta was completely suppressed by chloroethylclonidine, but only slightly inhibited by N-allylsecoboldine and by verapamil. Glibenclamide or charybdotoxin did not affect the relaxation induced by N-allylsecoboldine of aortic rings precontracted with phenylephrine. Neither the cGMP nor the cAMP content was changed by N-allylsecoboldine. We conclude that N-allylsecoboldine relaxes the rat aorta by blocking Ca2+ channels and that it also has an antagonistic effect at alpha 1-adrenoceptors.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1994

Aristolochic acids, aristolactam alkaloids and amides from Aristolochia kankauensis.

Fourteen aristolochic acid derivatives: ariskanins A-E, 3-hydroxy-4-methoxy-10-nitrophenanthrene-1-carboxylic acid methyl ester, aristolochic acid-II methyl ester, aristolochic acid-IV methyl ester, aristolochic acid-C, -I, -II, -III, -IV, -IVa; nine aristolactam alkaloids: aristolactam, aristolactam-AII, -BIII, -AIII, -III, cepharanone-A, 9-methoxy-aristolactam-I, aristolactam-N-beta-D-glucoside and aristolactam-C-N-beta-D-glucoside; a 4,5-dioxoaporphine alkaloid: cepharadione-A, together with 12 other compounds: methyl-p-coumarate, N-trans-feruloyltyramine, N-cis-feruloyltyramine, methyl vanillate, methyl paraben, allantoin, an octadecyl- and eicosyl ferulate mixture, cis- and trans-p-coumaric acid, N-p-coumaroyltyramine, N-p-cis-coumaroyltyramine, methyl ferulate and isorhamnetin-3-O-rutinoside were isolated and characterized from the fresh root and stem of Aristolochia kankauensis. Their structures were elucidated by spectral and chemical methods. Among them, ariskanins-A-E and N-p-cis-coumaroyltyramine are reported for the first time from a natural source. The cytotoxicity and antiplatelet activity of the compounds isolated are also discussed.

Alkaloids↗

PubMed1994

Antiplatelet constituents of formosan Rubia akane.

A known steroid, in addition to triterpenoids, anthraquinones, naphthalenes and a new anthraquinone glycoside, xanthopurpurin 3-O-beta-D-glucoside, were isolated from the roots of Rubia akane grown in Taiwan. Mollugin, a naphthohydroquinone, showed strong inhibition of arachidonic acid (AA)-induced and collagen-induced platelet aggregation. In contrast, 2-methyl-1,3,6-trihydroxyl-9,10-anthraquinone, xanthopurpurin 3-O-beta-D-glucoside, and xanthopurpurin showed mainly strong inhibition of collagen-induced platelet aggregation.

Animals↗