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Biomedical subjects

C M Teng

Publications and source records attributed to C M Teng.

At least 37 records · Page 2Linked to original sources
PubMed2000

Burst firing of action potentials in central snail neurons elicited by d-amphetamine: effect of anticonvulsants.

The effect of anticonvulsants on the burst firing of action potentials in snail central neuron elicited by d-amphetamine was studied in the identified RP4 neuron of the African snail, Achatina fulica Ferussac. Oscillation of membrane potential and burst firing of action potentials were elicited by d-amphetamine in a concentration-dependent manner. Voltage clamped studies revealed that d-amphetamine elicited a negative slope resistance (NSR) in steady-state I-V curve between - 40 and - 10 mV. The burst firing of action potentials was alleviated following extracellular application of phenytoin, but was not affected after ethosuximide, carbamazepine, and valproic acid. The NSR elicited by d-amphetamine was blocked by phenytoin. However, the NSR was not altered if carbamazepine was added. These results suggest that of the four anticonvulsants tested, only phenytoin could alleviate the burst firing of action potentials elicited by d-amphetamine in snail neuron.

Action Potentials↗
PubMed2000

Aristolactams and dioxoaporphines from Fissistigma balansae and Fissistigma oldhamii.

Investigation of extracts of Fissistigma balansae and Fissistigma oldhamii resulted in the isolation of 11 aristolactams-stigmalactam (1), piperolactam A (2), piperolactam C (3), aristolactam AII (4), aristolactam AIIIa (5), aristolactam BII (6), aristolactam BIII (7), aristolactam FII (8), goniothalactam (9), enterocarpam I (10), and velutinam (11)-as well as two dioxoaporphines, noraristolodione (12) and norcepharadione B (13). The new compound 1 was identified by spectral data interpretation. Compounds 1-13 were subjected to antiplatelet aggregation testing.

Animals↗
PubMed2000

YD-3, a novel inhibitor of protease-induced platelet activation.

1. In the present study, the antiplatelet effects and mechanisms of a new synthetic compound YD-3 [1-benzyl-3(ethoxycarbonylphenyl)-indazole] were examined. 2. YD-3 inhibited the aggregation of washed rabbit platelets caused by thrombin (IC(50)=28.3 microM), but had no or little inhibitory effect on that induced by arachidonic acid, collagen, platelet-activating factor (PAF) or U46619. YD-3 also suppressed generation of inositol phosphates caused by thrombin. On the other hand, thrombin-induced fibrin formation was not affected by YD-3, indicating YD-3 does not inhibit the proteolytic activity of thrombin. 3. In washed human platelets, however, YD-3 had only mild inhibitory effect on the low concentration (0.05 u ml(-1)) of thrombin-induced human platelet aggregation, and did not affect that induced by higher concentrations (> or =0.1 u ml(-1)) of thrombin or SFLLRN, the protease-activated receptor 1 (PAR1) agonist peptide. By contrast, YD-3 inhibited both human and rabbit platelet aggregation elicited by trypsin with IC(50) values of 38.1 microM and 5.7 microM, respectively. 4. YD-3, at 100 microM, had no effect on ristocetin-induced glycoprotein Ib (GPIb)-dependent aggregation of human platelets. In addition, platelets treated with chymotrypsin, which cleaves GPIb, enhanced rather than attenuated the inhibition of YD-3 on thrombin-induced human platelet aggregation. These data indicate that GPIb plays no role in the antiplatelet effect of YD-3. 5. In SFLLRN-desensitized human platelets, high concentration of thrombin (1 u ml(-1)) could still elicit intracellular Ca(2+) mobilization, and the rise of [Ca(2+)](i) was prevented by either leupeptin or YD-3. 6. Our results suggest that YD-3 inhibits a non-PAR1 thrombin receptor which mediates the major effect of thrombin in rabbit platelets, but in human platelets, this receptor function becomes significant only when the function of PAR1 has been blocked or attenuated.

Animals↗
PubMed2000

Antiplatelet aggregation principles from Ephemerantha lonchophylla.

Bioactivity-directed separation led to the identification of four compounds, viz. denbinobin (1), 3,7-dihydroxy-2,4-dimethoxyphenanthrene (2), 3-methylgigantol (3), and erianthridin (4) from the ethanolic extract of Ephemerantha lonchophylla. Antiplatelet tests were carried out using 4 different aggregation inducers, viz. arachidonic acid (AA), thrombin, collagen and platelet activating factor (PAF). The results indicated that only compounds 2, 3, and 4 exhibited generally significant anti-aggregation activities with that against AA-induced aggregation being most effective. Estimated IC50, values in this regard for 2, 3, and 4 were 24 microM, 30 microM and 9 microM, respectively.

Medicine, Chinese Traditional↗
PubMed2000

Anti-platelet aggregation alkaloids and lignans from Hernandia nymphaeifolia.

A new aporphine, N-(N-methylcarbamoyl)-O-methyl-bulbocapnine (1), together with seven known compounds, (-)-5'-methoxypodorhizol (2), a mixture of beta-sitosterone (3) and stigmasta-4,22-dien-3-one (4), a mixture of 3 beta-hydroxystigmast-5-en-7-one (5) and 3 beta-hydroxystigmasta-5,22-dien-7-one (6), and a mixture of 6 alpha-hydroxystigmast-4-en-3-one (7) and 6 alpha-hydroxystigmasta-4,22-dien-3-one (8), were isolated in continuing studies on the trunk bark of Formosan Hernandia nymphaeifolia. The structures of these compounds were determined through spectral analyses. In addition, the previously reported six alkaloids, laurotetanine, oxohernagine, thalicarpine, reticuline, (+)-vateamine-2'-beta-N-oxide, (+)-hernandaline and six lignans, (+)-epiaschantin, (+)-epimagnolin, (+)-epiyangambin, (-)-hernone, (-)-yatein, (-)-deoxypodophyllotoxin were demonstrated to have anti-platelet aggregation activity.

Alkaloids↗
PubMed2000

Coumarins and antiplatelet constituents from the root bark of Zanthoxylum schinifolium.

Further study on the chloroform-soluble portion of the root bark of Zanthoxylum schinifolium led to the isolation of eight new coumarins: methylschinilenol (1), hydroxyepoxycollinin I (2), 8-methoxyanisocoumarin H (3), hydroxyschininallylol (4), hydroxyepoxycollinin II (5), schinitrienin (6), schininallylone (7), and isoschinilenol (8), along with twenty-six known compounds including fourteen coumarins, and nine alkaloids. The structural elucidation was determined by spectroscopic data. Among the isolates, terpenyl-coumarins and furoquinolines were the active constituents with antiplatelet aggregation in vitro and collinin (10) showed significant anti-HBC DNA replication activity.

Coumarins↗
PubMed2000

Antiplatelet effect of marchantinquinone, isolated from Reboulia hemisphaerica, in rabbit washed platelets.

Platelet activation is involved in serious pathological situations, including atherosclerosis and restenosis. It is important to find efficient antiplatelet medicines to prevent fatal thrombous formation during the course of these diseases. Marchantinquinone, a natural compound isolated from Reboulia hemisphaerica, inhibited platelet aggregation and ATP release stimulated by thrombin (0.1 units mL(-1)), platelet-activating factor (PAF; 2 ng mL(-1)), collagen (10 microg mL(-1)), arachidonic acid (100 microM), or U46619 (1 microM) in rabbit washed platelets. The IC50 values of marchantinquinone on the inhibition of platelet aggregation induced by these five agonists were 62.0 +/- 9.0, 86.0 +/- 7.8, 13.6 +/- 4.7, 20.9 +/- 3.1 and 13.4 +/- 5.3 microM, respectively. Marchantinquinone inhibited thromboxane B2 (TxB2) formation induced by thrombin, PAF or collagen. However, marchantinquinone did not inhibit TxB2 formation induced by arachidonic acid, indicating that marchantinquinone did not affect the activity of cyclooxygenase and thromboxane synthase. Marchantinquinone did inhibit the rising intracellular Ca2+ concentration stimulated by the five platelet-aggregation inducers. The formation of inositol monophosphate induced by thrombin was inhibited by marchantinquinone. Platelet cAMP and cGMP levels were unchanged by marchantinquinone. The results indicate that marchantinquinone exerts antiplatelet effects by inhibiting phosphoinositide turnover.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Synthesis and anti-platelet, anti-inflammatory and anti-allergic activities of methoxyisoflavanquinone and related compounds.

In a continuation of our search for novel anti-platelet agents, isoflavone quinone and isoflavanquinone were selected as lead compounds and the synthesis of their methoxy derivatives was carried out. Among them, the 4'- and 7-methoxy derivatives were successfully prepared, whereas the attempt to obtain 3'-methoxy derivatives resulted in their isomers, 3'-methoxyflavone quinone and 3'-methoxyflavanquinone, instead. After screening for their anti-platelet, anti-inflammatory and anti-allergic activities, a preliminary structure-activity relationship was established. Compounds 6c, 7a-c, 8c and 9a-c were found to exhibit significant activities. In particular, compound 7c demonstrated very potent anti-platelet, anti-inflammatory and anti-allergic activities and was then recommended for further pharmacological investigation.

Animals↗
PubMed2000

Effects of ouabain on tension response and [3H]noradrenaline release in human prostate.

PURPOSE: The activity of Na+/K+ ATPase is a crucial factor in lots of functions of vascular and nonvascular smooth muscles. However, its role in muscle contractility of human prostate has not been well elucidated. In this context, we have examined the effect of ouabain on the contractile response and noradrenaline release in human prostate to clarify the role of cardiac glycoside in the pathophysiology of bladder outlet obstruction associated by benign prostatic enlargement. MATERIALS AND METHODS: Human prostatic tissues (n = 12) were obtained at operation from males by open prostatectomy (n = 2) or transurethral resection of the prostate (n = 10). The effect of ouabain on muscle contraction and [3H]noradrenaline release was studied in human prostatic tissue. The action mechanism following the administration of ouabain was also examined. RESULTS: Ouabain concentration-dependently induced a gradual contraction in human prostate and this delayed contraction was significantly blocked by prazosin other than the other receptor antagonists. In parallel experiments, ouabain also caused a concentration-dependent gradual increase in [3H]noradrenaline release, which was extracellular Ca2+-dependent. Furthermore, ouabain-induced [3H]noradrenaline release increased, in a concentration-dependent manner, with increasing Na+ concentrations from 25 to 140 mM. Moreover, K+-free Krebs solution could mimic the [3H]noradrenaline release action to ouabain. CONCLUSIONS: Ouabain may induce an increase in tension response in human prostate, and this effect is due mainly to an increase in noradrenaline release via an effect on the Na+-dependent Ca2+ influx system.

Cardiotonic Agents↗
PubMed1999

Antiplatelet actions of aporphinoids from Formosan plants.

Seventeen aporphines were tested for antiplatelet activity. L-(+)-hemovine HCl and 7-hydroxydehydrothalicsimidine strongly inhibited platelet aggregation induced by adenosine 5'-diphosphate (ADP), arachidonic acid (AA), collagen, and platelet-activating factor (PAF). The latter showed the strongest antiplatelet activity with an IC50 of 70.4 microM against AA-induced platelet aggregation.

Animals↗
PubMed1999

YC-1 potentiates the antiplatelet effect of hydrogen peroxide via sensitization of soluble guanylate cyclase.

In the present study, we showed that 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1), a nitric oxide (NO)-independent activator of soluble guanylate cyclase, could potentiate H2O2-induced inhibition of platelet aggregation and increase of platelet cGMP levels. The synergistic effect of YC-1 and H2O2 on platelet aggregation and increases of cGMP were almost completely prevented by catalase and a selective soluble guanylate cyclase inhibitor (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), or partially attenuated by the hydroxyl radical scavenger mannitol. In contrast, superoxide dismutase failed to influence H2O2/YC-1-induced inhibition of aggregation. Furthermore, YC-1 could enhance the activation of soluble guanylate cyclase caused by FeSO4/H2O2 and, this effect was prevented markedly by mannitol. These results suggest that YC-1 may enhance the antiaggregatory effect of H2O2 via the sensitization of platelet soluble guanylate cyclase. In addition, this phenomenon is, at least in part, dependent on H2O2-derived hydroxyl radical.

Antioxidants↗
PubMed1999

Investigation of the effects of some alkaloidal alpha1-adrenoceptor antagonists on human hyperplastic prostate.

The effects of N-allylsecoboldine, (-)-discretamine, ( )-govadine and [(+/-)-2,3,10,11-tetrahydroxytetrahydroproto-berberine HBr] ((+/-)-THP) on contractile responses were investigated in human hyperplastic prostate. They all inhibited, concentration dependently, the tension responses to phenylephrine and electrical field stimulation, and the pA2 and pIC50 values were calculated. The relative potencies of these four agents with reference to prazosin were obtained. The results showed that N-allylsecoboldine exhibited greater potency (4.1-fold), whereas (-)-discretamine, (+/-)-govadine and (+/-)-THP had similar potencies, against contractions elicited by electrical field stimulation and against contractions elicited by phenylephrine in human hyperplastic prostate. In addition, the potency ratios of N-allylsecoboldine, (-)-discretamine, (+/-)-govadine and (+/-)-THP against phenylephrine-induced contractions in rat vas deferens/spleen were 7.78, 0.89, 0.57, and 0.96, respectively. In the presence of prazosin (0.3 +/-M) to block alpha1-adrenoceptor-mediated responses, nifedipine (10 microM), but not the above four agents, significantly blocked KCl (60 mM)-induced tension responses in human hyperplastic prostate. It is suggested that N-allylsecoboldine exhibits greater potency against nerve-mediated contraction than against phenylephrine-induced contraction in human hyperplastic prostate and that this antagonistic effect is due mainly to its high affinity for the alpha1A-adrenoceptor subtype.

Adrenergic alpha-Antagonists↗
PubMed1999

Chronic hyperammonemia in rats impairs activation of soluble guanylate cyclase in neurons and in lymphocytes: a putative peripheral marker for neurological alterations.

Chronic hyperammonemia impairs the glutamate-nitric oxide-cGMP pathway in rat brain in vivo. The aims of this work were to assess whether hyperammonemia impairs modulation of soluble guanylate cyclase, and to look for a peripheral marker for impairment of this pathway in brain. We activated the pathway at different steps using glutamate, SNAP, or YC-1. In control neurons these compounds increased cGMP by 7.4-, 9.7- and 7.2-fold, respectively. In ammonia-treated neurons formation of cGMP induced by glutamate, SNAP, and YC-1 was reduced by 50%, 56%, and 52%, respectively, indicating that hyperammonemia impairs activation of guanylate cyclase. This enzyme is also present in lymphocytes. Activation of guanylate cyclase by SNAP or YC-1 was impaired in lymphocytes from hyperammonemic rats. These results suggest that determination of the activation of soluble guanylate cyclase in lymphocytes could serve as a peripheral marker for impairment of the neuronal glutamate-nitric oxide-cGMP pathway in brain.

Ammonia↗
PubMed1999

Inhibition of 2-P-mercaptophenyl-1,4-naphthoquinone on human platelet function.

As widely assumed, platelets and coagulation system heavily influence the pathogenesis and progression of cardiovascular diseases. Some 1,4-naphthoquinone derivatives, such as vitamin K3, have been reported to increase the synthesis of coagulation proteins. In this study, we examine how 2-p-mercaptophenyl -1,4-naphthoquinone (NTP), a newly synthesized 1,4-naphthoquinone derivative, affects the platelet function in humans. A tapered parallel plate chamber which provided a range of shear stress covering the entire physiological range in human circulation is used to assess platelet adhesiveness on fibrinogen coated-surface. In addition, platelet aggregation and thromboxane B2 (TXB2) production by inducers are evaluated by the turbidimetric method and enzyme immunoassay kit, respectively. Moreover, platelets [Ca2+]i are measured using a dual-wavelength fluorescence spectrophotometer. Analysis results indicate that 1) NTP decreases the percentages of attached platelets at the locations in various shear stresses and the levels of platelet adhesiveness, denoted as the slope; 2) NTP can inhibit the platelet aggregation by ADP (2 microM) and collagen (25 microg/ml), and the IC50 are: 0.32 and 26.83 microg/ml, respectively; and 3) NTP markedly inhibits TXB2 formation and platelet [Ca2+]i elevation caused by ADP and collagen. Therefore, we conclude that NTP may inhibit platelet adhesiveness on fibrinogen coated-surface, aggregability, [Ca2+]i, and thromboxane production, and that it may be used as an antiplatelet agent.

Adenosine Diphosphate↗
PubMed1999

Studies on the cardiovascular action of TPY-beta: an antihypertensive agent with antiplatelet activity.

1-Pyrrolidinylmethyl-2-naphthol hydrochloride (TPY-beta) has been reported to have hypotensive and bradycardiac effects in anesthetized rats. Whether administration of atropine or bilateral vagotomy affects mean arterial pressure or heart rate was examined. The percentage difference in hypotensive and bradycardiac effect of TPY-beta (0.5 mg/kg) was 63 +/- 5% and 68 +/- 9%, respectively, in unpretreated rats compared to control levels. Atropine pretreatment (0.1 mg/kg, i.v.) significantly reduced the depressant effect of TPY-beta, although heart rate and mean arterial pressure remained 21 +/- 3% and 31 +/- 4%, respectively, as compared to control levels. Vagotomy decreased heart rate and mean arterial pressure response but moderate bradycardiac (13 +/- 2%) and hypotensive (10 +/- 3%) effects still remained as compared to control levels. Unilateral microinjection of 1, 3.3 and 10 nM TPY-beta into the nucleus tractus solitarri elicited a dose-dependent depressor (-10 +/- 2; -20 +/- 3; -25 +/- 3 mmHg) and bradycardiac activities (-20 +/- 4; -26 +/- 5; -55 +/- 10 beats/min). TPY-beta also relaxed the isolated rat aortic rings preconstracted with high extracellular K+ (80 mM) and Ca2+ (1.9 mM). The above findings suggest that the suppressive effects of TPY-beta may involve activation of vagus nerve and a direct inhibition of Ca2+ channel. In addition, TPY-beta inhibited the aggregation of washed rabbit platelets (aggregated by arachidonic acid and collagen) and adhesiveness on fibrinogen-coated surface. The results suggest that TPY-beta possesses antihypertensive and antiplatelet activity.

Animals↗
PubMed1999

Chemical constituents and biological activities of the fruit of Zanthoxylum integrifoliolum.

Through continuing studies on the chemical constituents and antiplatelet aggregation principles of the fruit of the Formosan Zanthoxylum integrifoliolum, four new compounds-including two new lignans, (+)-pinoresinol-di-3,3-dimethylallyl ether (1), and (+)-pinoresinol-3,3-dimethylallyl ether (2); zanthonitrile (3), and one new flavonoid, 3,5-diacetyltambulin (4)-and 18 known compounds were isolated from the CHCl3-soluble fraction. Their structures were elucidated on the basis of spectral data and chemical evidence. Among the isolates, including the previously reported isobutylamides, 13 compounds showed strong in vitro antiplatelet aggregation activity, with only (-)-tetrahydroberberine showing weak vasorelaxing effect in high potassium- or norepinephrine-induced contraction of rat aorta.

Animals↗
PubMed1999

YC-1 potentiates nitric oxide-induced relaxation in guinea-pig trachea.

1. The effects of YC-1 (3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole) on tension, levels of cyclic GMP and cyclic AMP were investigated in guinea-pig trachea. We especially studied the combined effect of YC-1 with exogenous or endogenous nitric oxide on these parameters. 2. YC-1 at the concentration 3 or 10 microM, which caused only minor effect by itself, elicited concentration-dependent potentiation of sodium nitroprusside (SNP)-induced tracheal relaxation. This relaxation of YC-1 with SNP was reversed by ODQ. 3. Relaxant responses to electric field stimulation (EFS) in the presence of indomethacin, atropine, guanethidine, alpha-chymotrypsin and histamine were also markedly increased by YC-1 (10 microM). In the presence of L-NAME or ODQ, the relaxant effects to EFS were attenuated and the following addition of YC-1 did not further enhance relaxation. 4. YC-1 (10 microM) or SNP (0.3 microM) alone did not induce significant elevation of cyclic GMP levels in the presence of IBMX, whereas simultaneous application of both compounds markedly elevated the cyclic GMP accumulation. In contrast, the cyclic AMP levels were not altered even at the combination of YC-1 and SNP. Additionally, YC-1 also affected cyclic GMP metabolism, since it inhibited the activity of phosphodiesterase type V in human platelets. 5. YC-1 (30 microM) did not scavenge superoxide anion and had no effect on the removal of superoxide anion by superoxide dismutase in a xanthine/xanthine oxidase system. 6. In conclusion, these results indicate that although YC-1 elicits negligible relaxation of guinea-pig trachea by itself, it can potentiate the relaxant responses of exogenous or endogenous NO. This synergistic response of YC-1 is via the elevation of cyclic GMP contents.

Animals↗