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Biomedical subjects

C M Teng

Publications and source records attributed to C M Teng.

At least 217 records · Page 12Linked to original sources
PubMed1990

Chlorobutanol, a preservative of desmopressin, inhibits human platelet aggregation and release in vitro.

Therapeutic preparations of desmopressin for parenteral use contain the preservative chlorobutanol (5 mg/ml). We show here that chlorobutanol is a potent inhibitor of platelet aggregation and release. It exhibited a significant inhibitory activity toward several aggregation inducers in a concentration- and time-dependent manner. Thromboxane B2 formation, ATP release, and elevation of cytosolic free calcium caused by collagen, ADP, epinephrine, arachidonic acid and thrombin respectively were markedly inhibited by chlorobutanol. Chlorobutanol had no effect on elastase-treated platelets and its antiplatelet effect could be reversed. It is concluded that the antiplatelet effect of chlorobutanol is mainly due to its inhibition on the arachidonic acid pathway but it is unlikely to have a nonspecific toxic effect. This antiplatelet effect of chlorobutanol suggests that desmopressin, when administered for improving hemostasis, should not contain chlorobutanol as a preservative.

Adenosine Triphosphate↗
PubMed1990

Comparison of the enzymatic and edema-producing activities of two venom phospholipase A2 enzymes.

The edema-producing activity of NNAVPLA2, an acidic phospholipase A2 (PLA2) enzyme from Naja naja atra venom (NNAV), was less potent than that of TMVPLA2 II, a basic PLA2 from Trimeresurus mucrosquamatus venom (TMV). These edema-forming effects were greatly suppressed by pretreatment of rats with diphenhydramine/methysergide or compound 48/80, which reduced the tissue content of histamine and serotonin. Heparin abolished and suppressed the paw edema caused by protamine and TMVPLA2 II, respectively, but had no effect on the NNAVPLA2-induced response. In isolated rat peritoneal mast cells, both PLA2 concentration dependently induced the release of histamine and beta-glucuronidase. Again, TMVPLA2 II was more potent than NNAVPLA2. This degranulation effect of mast cells caused by TMVPLA2 II and protamine was inhibited by heparin, while that caused by NNAVPLA2 was unaffected. The edema-forming and mast cell degranulation effects were greatly decreased in both PBPB-modified NNAVPLA2 and PBPB-modified TMVPLA2 II, in which the catalytic activity of the enzymes was completely lost. PBPB-modified TMVPLA2 II-induced paw edema was also suppressed by heparin. Furthermore, this edematous response was totally reversed in rat pretreated with aspirin in combination with diphenhydramine and methysergide. These results suggest that the edema-forming effect of PLA2 is probably dependent on the presence of catalytic, positive charge and pharmacological sites on its molecule.

Animals↗
PubMed1990

A simple method to create carotid endothelial laceration and acute platelet thrombus in vivo in guinea-pig.

A simple method, named 'clamp method', was developed to create carotid endothelial laceration and produce acute platelet thrombus in vivo in guinea-pig. This method used a hemostatic forceps to clamp common carotid artery of anesthetized guinea-pig at a tangent angle. Our study included two parts. The Part one demonstrated the procedures and effects of the 'clamp method': sixteen guinea-pigs were divided equally into control and heparin-treated groups. These two groups received the same clamping procedures except that the heparin-treated group was administrated with heparin (5,000U/kg) intravenously before clamping. One hour after the clamping, carotid arteries were resected and observed under scanning electron microscopy. The results showed that large carotid mural thrombi were formed in the control group with a mean surface area of 1.75 +/- 0.63 mm2 (M +/- SD, n = 8). In the heparin-treated group, the thrombus formation was prevented and linear endothelial lacerations were seen clearly. The Part two of our study identified the histologic nature of the thrombus produced by the 'clamp method': eight guinea-pigs received same procedures as that of control group in the Part one except that the carotid arteries were resected 5 min after performing the clamping. Four of the eight specimens were prepared for observation under transmission electron microscopy. The results showed that platelets adhered onto the subendothelial substances and formed platelet thrombi in the endothelial lacerations within 5 min after the carotid clamping.

Animals↗
PubMed1990

Vasorelaxing effect in rat thoracic aorta caused by denudatin B, isolated from the Chinese herb, magnolia fargesii.

Denudatin B is an antiplatelet agent isolated from the flower buds of Magnolia fargesii. We studied the effects of denudatin B on the vasoconstriction of rat thoracic aorta induced by high potassium (K+) solution, norepinephrine (NE) and caffeine, and to elucidate its mode of action. The contraction of rat aorta caused by high K+ (60 mM) and cumulative concentrations of CaCl2 (0.03-3 mM) was inhibited concentration dependently by denudatin B with an IC50 of 21.2 micrograms/ml. NE (3 microM)-induced phasic and tonic contractions of rat aorta were inhibited by pretreatment with denudatin B (10-100 micrograms/ml). The relaxing action of denudatin B persisted in denuded aorta, in Ca2(+)-free and EGTA (2 mM)-containing medium. The vasorelaxing effects were not affected by indomethacin (20 microM), hemoglobin (10 microM) or methylene blue (50 microM) and were not accompanied by PGI2 formation. In quin-2/AM-loaded cultured rat vascular smooth muscle cells, denudatin B (100 micrograms/ml) inhibited the increase of intracellular calcium caused by NE (3 microM) in the presence or absence of extracellular calcium. Denudatin B did not affect the caffeine (10 mM)-induced contraction and the increase in intracellular calcium. Denudatin B (100 micrograms/ml) increased the cGMP, but not the cAMP level in intact and denuded aorta. The 45Ca2+ influx induced in rat aorta by high K+ (60 mM) or NE (3 microM) was markedly inhibited by denudatin B in a concentration-dependent manner. These results indicate that denudatin B relaxed vascular smooth muscle by inhibiting the Ca2+ influx through voltage-gated and receptor-operated Ca2+ channels; its effect to increase cGMP may enhance the vasorelaxation.

Animals↗
PubMed1990

Inhibition of thrombin- and collagen-induced phosphoinositides breakdown in rabbit platelets by a PAF antagonist--denudatin B, an isomer of kadsurenone.

Denudatin B, an isomer of kadsurenone, was isolated from Magnolia fargesii. It inhibited the aggregation and ATP release of washed rabbit platelets caused by platelet-activating factor (PAF) in a concentration-dependent manner. The IC50 on PAF (2 ng/ml)-induced aggregation was about 10 micrograms/ml. High concentration of denudatin B (greater than 50 micrograms/ml) also inhibited the aggregation and ATP release of platelets caused by ADP, collagen, arachidonic acid and thrombin. However, shape change of platelets still existed. Prolongation of the incubation time with platelets could not cause further inhibition, and the aggregability of platelets could be restored after denudatin B was washed out from platelets. Thrombin-induced thromboxane B2 formation was almost completely suppressed. In the absence of extracellular calcium (EGTA 1 mM), ATP release caused by thrombin was inhibited. Thrombin-induced rise of the intracellular calcium concentration was suppressed by denudatin B, but not by BN52021 or kadsurenone. The generation of inositol phosphate in washed platelets caused by collagen, PAF and thrombin was also suppressed. The data indicate that PAF antagonist denudatin B has nonspecific antiplatelet action at high concentration by inhibiting phosphoinositides breakdown induced by collagen and thrombin.

Animals↗
PubMed1990

Antiplatelet effects of chelerythrine chloride isolated from Zanthoxylum simulans.

Chelerythrine chloride is an antiplatelet agent isolated from Zanthoxylum simulans. Aggregation and ATP release of washed rabbit platelets caused by ADP, arachidonic acid, PAF, collagen, ionophore A23187 and thrombin were inhibited by chelerythrine chloride. Less inhibition was observed in platelet-rich plasma. The thromboxane B2 formation of washed platelets caused by arachidonic acid, collagen, ionophore A23187 and thrombin was decreased by chelerythrine chloride. Phosphoinositides breakdown caused by collagen and PAF was completely inhibited by chelerythrine chloride, while that of thrombin was only partially suppressed. Chelerythrine chloride inhibited the intracellular calcium increase caused by arachidonic acid, PAF, collagen and thrombin in quin-2/AM-loaded platelets. The cyclic AMP level of washed platelets did not elevated by chelerythrine chloride. The antiplatelet effect of chelerythrine chloride was not dependent on the incubation time and the aggregability of platelets inhibited by chelerythrine chloride was easily recovered after sedimenting the platelets by centrifugation and then the platelet pellets were resuspended. Chelerythrine chloride did not cause any platelet lysis, since lactate dehydrogenase activity was not found in the supernatant. These data indicate that the inhibitory effect of chelerythrine chloride on rabbit platelet aggregation and release reaction is due to the inhibition on thromboxane formation and phosphoinositides breakdown.

Adenosine Triphosphate↗
PubMed1990

Inhibition of rabbit platelet aggregation by 1,4-naphthoquinones.

The effects of four 1,4-naphthoquinone derivatives on the aggregation of rabbit platelets were examined. All the four 1,4-naphthoquinone derivatives inhibited the platelet aggregation of washed rabbit platelets induced by thrombin (0.1 U/ml) and the IC50 is: 2-chloro-3-methyl-1,4-naphthoquinone (CMN), 5 micrograms/ml; 3-methyl-5,8-dihydroxy-1,4-naphthoquinone, 13 micrograms/ml; 5,8-dihydroxy-1,4-naphthoquinone, 18 micrograms/ml; 3-methyl-1,4-naphthoquinone (vitamin K3), 53 micrograms/ml. CMN was the most potent in inhibiting the aggregation and release reaction induced by ADP, arachidonic acid, PAF, ionophore A23187, collagen and thrombin in a dose-dependent manner in washed platelets, platelet-rich-plasma and whole blood. The thromboxane B2 formation caused by collagen and ionophore A23187 was inhibited by CMN. However, the thromboxane B2 formation by arachidonic acid was markedly increased. The platelet inhibitory effect of CMN could not be antagonized either by raising the concentrations of extracellular Ca++ or by wash out. The phosphoinositides breakdown induced by thrombin was inhibited by CMN. Phospholipids (PE, PC, PI) could slightly antagonize the antiplatelet effect of CMN. It is concluded that the inhibitory effect of CMN on rabbit platelet aggregation may be due to the inhibition of phosphoinositides breakdown caused by the inducers.

Adenosine Diphosphate↗
PubMed1990

EDRF-release and Ca+(+)-channel blockade by magnolol, an antiplatelet agent isolated from Chinese herb Magnolia officinalis, in rat thoracic aorta.

Magnolol is an antiplatelet agent isolated from Chinese herb Magnolia officinalis. It inhibited norepinephrine (NE, 3 microM)-induced phasic and tonic contractions in rat thoracic aorta. At the plateau of the NE-induced tonic contraction, addition of magnolol caused two phases (fast and slow) of relaxation. These two relaxations were concentration-dependent (10-100 micrograms/ml), and were not inhibited by indomethacin (20 microM). The fast relaxation was completely antagonized by hemoglobin (10 microM) and methylene blue (50 microM), and disappeared in de-endothelialized aorta while the slow relaxation was not affected by the above treatments. Magnolol also inhibited high potassium (60 mM)-induced, calcium-dependent (0.03 to 3 mM) contraction of rat aorta in a concentration-dependent manner. 45Ca(+)+ influx induced by high potassium or NE was markedly inhibited by magnolol. Cyclic GMP, but not PGI2, was increased by magnolol in intact, but not in de-endothelialized aorta. It is concluded that magnolol relaxed vascular smooth muscle by releasing endothelium-derived relaxing factor (EDRF) and by inhibiting calcium influx through voltage-gated calcium channels.

Animals↗
PubMed1990

Antiplatelet components in Panax ginseng.

Panaxynol and ginsenosides Ro, Rg1, and Rg2 were found to be the main antiplatelet components in the diethyl ether and 1-butanol fractions, respectively, during the activity-guided fractionation of Panax ginseng, Panaxynol inhibited the aggregation, release reaction, and thromboxane formation in rabbit platelets while ginsenosides Ro, Rg1, and Rg2 suppressed the release reaction only.

Animals↗
PubMed1990

Effect of anti-inflammatory drugs on the cardiotoxin-induced hind-paw oedema in rats.

Cardiotoxin, isolated from Naja naja atra venom, induced rat hind-paw oedema. This effect was suppressed by the pretreatment with dexamethasone or BW 755C, or subplantar co-injection with FPL 55712. Pretreatment with aspirin alone did not affect this response, while a significant reduction of cardiotoxin-induced paw oedema was achieved with aspirin in combination with diphenhydramine and methysergide. Subplantar co-injection of PAF antagonist, BN 52021 or L 652731, with cardiotoxin had no effect on paw oedema, whereas superoxide dismutase/catalase reduced this oedematous response. Cardiotoxin-induced paw oedema was also suppressed by pretreating the rats with isoprenaline. Pretreatment with rat anti-platelet plasma, which greatly reduced peripheral platelet count, did not affect cardiotoxin-induced paw oedema. Cardiotoxin did not trigger platelet aggregation or release reaction either in platelet-rich plasma or in washed platelet suspension. The oedematous response after subplantar co-injection of cardiotoxin with basic or acidic phospholipase A2 appeared to be only an additive effect. These results suggest that arachidonate metabolites, in which leukotrienes are most important, participated in cardiotoxin-induced paw oedema. Superoxide radical was also involved, while PAF and platelets showed little influence in this oedema effect.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1990

Rat paw oedema and mast cell degranulation caused by two phospholipase A2 enzymes isolated from Trimeresurus mucrosquamatus venom.

Two phospholipase A2 (PLA2) enzymes, TMVPLA2 I and TMVPLA2 II, isolated from Trimeresurus mucrosquamatus venom (TMV) induce rat hind-paw oedema in a dose-dependent manner. This response is suppressed by pretreatment with diphenhydramine, methysergide or compound 48/80, which reduces tissue histamine content. In isolated mast cells, TMVPLA2 I and TMVPLA2 II cause concentration-, time- and calcium-dependent release of histamine and beta-glucuronidase. This effect is inhibited by disodium cromoglycate, mepacrine, nordihydroguaiaretic acid, piriprost and BW 755C, but not by aspirin or indomethacin. These observations indicate that the mast cell plays a predominant role in TMVPLA2 I- and TMVPLA2 II-induced paw oedema, and that venom PLA2 enzyme needs an intact lipoxygenase pathway to induce mast cell degranulation.

Animals↗
PubMed1990

Antiplatelet action of dehydrokawain derivatives isolated from Alpinia speciosa rhizoma.

5,6-Dehydrokawain (DK) and dihydro-5,6-dehydrokawain (DDK) inhibited the aggregation and ATP release of rabbit platelets induced by arachidonic acid and collagen, without affecting those induced by ADP, PAF and thrombin. This inhibition was reversible and in a concentration-dependent manner. The IC50 of DK and DDK on arachidonate-induced platelet aggregation were calculated to be about 10 and 60 micrograms/ml, respectively. Thromboxane B2 formation caused by arachidonic acid was also suppressed by both antiplatelet agents. DK inhibited the intracellular calcium concentration rised by arachidonic acid, but not that by collagen or thrombin. DK also inhibited the secondary, but not the primary aggregation of human platelet-rich plasma induced by ADP and epinephrine. It is concluded that the antiplatelet effect of both DK and DDK is due to the inhibition of thromboxane A2 formation.

Adenosine Triphosphate↗
PubMed1989

Inhibition of platelet thromboxane formation and phosphoinositides breakdown by osthole from Angelica pubescens.

Osthole, isolated from Chinese herb Angelica pubescens, inhibited platelet aggregation and ATP release induced by ADP, arachidonic acid, PAF, collagen, ionophore A23187 and thrombin in washed rabbit platelets. It showed a weak activity in platelet-rich plasma. Osthole inhibited the thromboxane B2 formation caused by arachidonic acid, collagen, ionophore A23187 and thrombin in washed platelets, and also the thromboxane B2 formation caused by the incubation of lysed platelet homogenate with arachidonic acid. The generation of inositol phosphates in washed platelets caused by collagen, PAF and thrombin was suppressed by osthole. These data indicate that the inhibitory effect of osthole on platelet aggregation and release reaction was due to the inhibition of thromboxane formation and phosphoinositides breakdown.

Adenosine Triphosphate↗
PubMed1989

Novel inhibitory actions on platelet thromboxane and inositolphosphate formation by xanthones and their glycosides.

Xanthones and their glycosides were tested for their antiplatelet activities in washed rabbit platelets. Tripteroside acetate and norathyriol acetate were the most potent inhibitors. Tripteroside acetate inhibited platelet aggregation and ATP release induced by ADP, arachidonic acid, platelet-activating factor (PAF), collagen, ionophore A23187 and thrombin. The IC50 values of tripteroside acetate toward arachidonic acid- (100 microM) and collagen- (10 micrograms/ml) induced platelet aggregation were 10 and 30 micrograms/ml respectively. It inhibited thromboxane B2 formation of washed platelets caused by arachidonic acid, collagen, thrombin and ionophore A23187 and also that caused by the incubation of lysed platelet homogenate with arachidonic acid. Tripteroside acetate decreased the formation of inositolphosphate caused by thrombin, collagen and PAF, whereas it had no direct effect on fibrinogen-platelet interaction. It is concluded that xanthone derivatives inhibited platelet aggregation and release reaction by diminishing thromboxane formation and phosphoinositide breakdown.

Adenosine Diphosphate↗
PubMed1989

Antiplatelet effects of protopine isolated from Corydalis tubers.

Protopine inhibited the aggregation and ATP release of rabbit platelets induced by ADP, arachidonic acid, PAF, collagen and ionophore A23187. Although the platelet aggregation caused by thrombin was not inhibited by protopine (100 micrograms/ml), the release reaction was partially suppressed. In rabbit platelet-rich plasma, protopine also inhibited the platelet aggregation caused by ADP, arachidonic acid, PAF and collagen. The thromboxane B2 formation of washed platelets caused by arachidonic acid, collagen, ionophore A23187 and thrombin was suppressed by protopine. Protopine inhibited the intracellular calcium increase caused by arachidonic acid in quin-2/AM loaded rabbit platelets. In the presence of indomethacin, the intracellular calcium increase caused by collagen and PAF was completely suppressed by protopine, and the intracellular calcium increase caused by thrombin was partially inhibited. The phosphoinositides breakdown caused by collagen and PAF was inhibited by protopine, but that by thrombin was not affected significantly. Protopine did not cause the elevation of cyclic AMP level of platelets. It is concluded that the antiplatelet effects of protopine is due to inhibition on thromboxane formation and phosphoinositides breakdown and then lead to the decrease of intracellular calcium concentration.

Adenosine Triphosphate↗
PubMed1989

Triwaglerin: a potent platelet aggregation inducer purified from Trimeresurus wagleri snake venom.

Trimeresurus wagleri venom is the most potent inducer of platelet aggregation among the seven Trimeresurus snake venoms tested. By means of CM-Sephadex C-50 column chromatography, T. wagleri venom was separated into 19 fractions. Fraction XVI possessed the strongest aggregating activity and was further purified by Sephadex G-75 and on heparin-agarose columns, and finally Triwaglerin, with a molecular weight of 68000, was obtained. Its aggregating and ATP-releasing activity was dose-dependent and 10-times more potent than the crude venom. Triwaglerin was devoid of any of the enzymatic activities possessed by the crude venom. Triwaglerin-induced aggregation was not affected by indomethacin, creatine phosphate/creatine phosphokinase (CP/CPK), platelet-activating factor (PAF) antagonists, verapamil or heparin, but was inhibited completely by mepacrine, imipramine and forskolin and markedly by tetracaine and sodium nitroprusside. Thromboxane B2 formation caused by Triwaglerin was suppressed by mepacrine, imipramine and indomethacin. R59022 and TMB-8 caused a synergistic inhibitory effect against Triwaglerin-induced aggregation. These data suggest that Triwaglerin activates platelets in a unique action which is independent of formation of thromboxane A2 and PAF, or release of ADP.

Animals↗
PubMed1989

Antiplatelet actions of panaxynol and ginsenosides isolated from ginseng.

The antiplatelet effect of panaxynol isolated from the diethyl ether layer was compared with those of ginsenosides from the butanol layer of Panax ginseng. Panaxynol (0.1 mg/ml) inhibited markedly the aggregation of washed platelets induced by collagen, arachidonic acid, ADP, ionophore A23187, PAF and thrombin while ginsenosides had no significant effect on the aggregation but ginsenoside Ro (1 mg/ml) inhibited the ATP release of platelets. Less inhibitory effect of panaxynol was observed in the aggregation of platelet-rich plasma. Thromboxane B2 formation of platelets was inhibited by panaxynol but not by ginsenosides. The antiplatelet effect of panaxynol was dependent on the incubation time and the aggregability of platelets inhibited by panaxynol could not easily be recovered after washing the platelets. In human platelet-rich plasma, panaxynol prevented secondary aggregation and completely blocked ATP release from platelets induced by epinephrine and ADP. Both panaxynol and ginsenoside Rg2 inhibited the rise of intracellular calcium caused by collagen. It is concluded that panaxynol is the most potent antiplatelet agent in ginseng and its mechanism of action is chiefly due to the inhibition of thromboxane formation.

Adenosine Triphosphate↗