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T F Huang

Publications and source records attributed to T F Huang.

At least 109 records · Page 6Linked to original sources
PubMed1991

Dicentrine, a natural vascular alpha 1-adrenoceptor antagonist, isolated from Lindera megaphylla.

1. The pharmacological activity of dicentrine, isolated from Lindera megaphylla, was determined in rat isolated thoracic aorta, guinea-pig isolated trachea and human platelet-rich plasma. 2. Dicentrine was found to be a potent alpha 1-adrenoceptor blocking agent in rat thoracic aorta as revealed by its competitive antagonism of noradrenaline- (pA2 = 8.19 +/- 0.09) or phenylephrine (pA2 = 9.01 +/- 0.10)-induced vasoconstriction. These effects still persisted in denuded aorta. It was less potent than prazosin (pA2 = 10.60 +/- 0.10), but was more potent than phentolamine (pA2 = 7.53 +/- 0.10) or yohimbine (pA2 = 6.20 +/- 0.05). 3. Inositol monophosphate formation induced by noradrenaline (3 microM) in rat thoracic aorta was suppressed by dicentrine (3-10 microM) and prazosin (3 microM). 4. A high concentration of dicentrine (30 microM) did not affect the aortic contraction induced by the thromboxane receptor agonist U-46619 (1 microM), angiotensin II (1 microM), high potassium (60 mM) or carbachol (3 microM). 5. Contraction of guinea-pig trachea caused by histamine or carbachol was slightly inhibited by dicentrine (30 microM), while beta-adrenoceptor relaxation to isoprenaline in trachea was not affected. 6. Aggregation in human platelet-rich plasma induced by adrenaline (10 microM) was blocked by yohimbine (5 microM). A high concentration of dicentrine (greater than 30 microM) caused slight inhibition of aggregation, the release reaction and thromboxane formation. Complete blockade was obtained with 150 microM dicentrine. 7. It is concluded that dicentrine is a potent, selective alpha 1-adrenoceptor antagonist in vascular smooth muscle.

Adrenergic alpha-Antagonists↗
PubMed1991

Antihaemostatic and antithrombotic effect of some antiplatelet agents isolated from Chinese herbs.

Five antiplatelet agents have been isolated from Chinese herbs. Apigenin and magnolol are inhibitors of thromboxane synthesis, while osthole, protopine and norathyriol are inhibitiors of phosphoinositide breakdown. Thirty min after intraperitoneal (i.p.) administration of these drugs, tail bleeding time of mice was prolonged markedly in a dose-dependent manner by norathyriol, protopine, osthole and magnolol, but not by apigenin. However, the antiplatelet agents (up to 200 mg kg-1, i.p.) could not prevent acute thromboembolic death in mice. In endotoxin-induced experimental disseminated intravascular coagulation in rats, norathyriol (50-100 mg kg-1, i.p.) prevented the decrease in platelet counts and fibrinogen, and the prolongation of plasma prothrombin time. Norathyriol (100 mg kg-1, i.p.) also suppressed ex-vivo platelet aggregation induced by collagen and ADP in rat plasma.

Animals↗
PubMed1991

Triflavin, an antiplatelet Arg-Gly-Asp-containing peptide, is a specific antagonist of platelet membrane glycoprotein IIb-IIIa complex.

Triflavin, an antiplatelet peptide containing Arg-Gly-Asp, purified from Trimeresurus flavoviridis venom, inhibits aggregation of human platelets stimulated by a variety of agonists. It blocks aggregation through interference with fibrinogen binding to its specific receptor on the platelet surface membrane in a competitive manner, but it has no apparent effect on intracellular events, such as thromboxane B2 formation, phosphoinositides breakdown and intracellular Ca2+ mobilization of thrombin-activated platelets. In this study, we determined the complete sequence of triflavin, which is composed of a single polypeptide chain of 70 amino acids. Its sequence is rich in cysteine and contains Arg-Gly-Asp at residues 49-51 in the carboxy-terminal domain. Triflavin shows about 68% identity of amino acid sequence with trigramin, which is a specific antagonist of the fibrinogen receptor associated with glycoprotein IIb/IIIa complex. [125I]Triflavin binds to unstimulated and ADP-stimulated platelets in a saturable manner and its Kd values are estimated to be 76 and 74 nM, respectively; the corresponding numbers of binding sites are 31,029 and 34,863 per platelet, respectively. [125I]Triflavin binding is blocked by Gly-Arg-Gly-Asp-Ser in a competitive manner. EDTA, the Arg-Gly-Asp-containing peptides (including naturally occurring polypeptides, trigramin and rhodostomin), and monoclonal antibody, 7E3, raised against GP IIb/IIIa complex, inhibit [125I]triflavin binding to unstimulated and ADP-stimulated human platelets. In conclusion, triflavin specifically binds to fibrinogen receptor associated with GP IIb/IIIa complex and its binding site is located at or near GP IIb/IIIa complex, overlapping with those of 7E3 and another Arg-Gly-Asp-containing polypeptide, rhodostomin.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1991

Drug effects on myocardial ischemia- and reperfusion-induced arrhythmias in anesthetized rats.

The effects of drugs on ischemia and reperfusion-induced arrhythmias were studied in vivo in anesthetized rats. The chest was opened under artificial respiration and the heart was exposed. The left anterior descending coronary artery was occluded, followed by reperfusion for 10 min each. The drugs (mannitol 10-50 mg/kg, aspirin 0.25-5 mg/kg, verapamil 5-50 micrograms/kg and propranolol 1 mg/kg iv) were tested in the vagotomized animals. The test agent was dissolved in saline and 0.5 ml infused 15 min before the coronary occlusion. The results indicated that mannitol and aspirin reduced the incidence and duration of arrhythmias (ventricular premature contraction, ventricular tachycardia and ventricular fibrillation) during ischemia and reperfusion, while verapamil and propranolol reduced the incidence of arrhythmias during ischemia.

Animals↗
PubMed1991

The effect of microinjection of amino acids into the nucleus tractus solitarius on the diving bradycardia in the rat.

The role of nucleus tractus solitarius (NTS) in the diving bradycardia was studied in anesthetized rats. The floor of the 4th ventricle of the medulla was exposed and 0.1 microliters of the test agent was injected into NTS bilaterally. The simulated diving (head immersion) for 30 sec was performed before and after the injection. Blood pressure and heart rate were monitored. Before the treatment, heart rate decreased by 51% and blood pressure rose by 23% during the diving in the pooled data (n = 35). Injection of glutamate (0.1-1 mM) or CaCl2 (100 mM) into NTS attenuated the diving bradycardia, but that of GABA (0.1 mM), glycine (0.1 mM), KCl (100 mM) or saline solution did not affect the diving bradycardia significantly. Lesions of NTS also attenuated the diving bradycardia. These data suggest that NTS may play a role in modulation of the diving response.

Amino Acids↗
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

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

Disintegrins: a family of integrin inhibitory proteins from viper venoms.

Disintegrins represent a new class of low molecular weight, RGD-containing, cysteine-rich peptides isolated from the venom of various snakes. They interact with the beta 1 and beta 3 families of integrins and their potency is at least 500-2000 times higher than short RGDX peptides. Analysis of the amino acid sequences of 14 different disintegrins suggests that the RGD sequence, in the spatial configuration determined by the appropriate pairing of the cysteine residues, functions as a cell recognition site. However, certain nonconserved amino acids appear to modify the activity of disintegrins, their specificity for various receptors, and their ability to compete specifically with various ligands.

Amino Acid Sequence↗
PubMed1990

Recombinant bivalent live vaccines against neonatal colibacillosis in piglets.

The genes of colonization factor K88 and avirulent heat-labile enterotoxin LT A-B+ of enterotoxigenic E. coli (ETEC) have been ligated, and a vaccine strain containing recombinant plasmid that efficiently expresses two antigens has been obtained. Using the activity of beta-galactosidase as a selection marker instead of drug resistance, another bivalent vaccine strain with the same expression level has also been constructed. The vaccine strains have no toxicity and do not cause any adverse reactions. In challenge study and field trials, a high degree of protection from colibacillosis was afforded to piglets when their dams were immunized orally or parenterally. Practice of bivalent live vaccines including colonization factor and enterotoxin antigens and without antibiotic resistance gene shows effective.

Adhesins, Escherichia coli↗
PubMed1990

Effect of mannitol, n-2-mercaptopropionyl glycine and sodium nitroprusside on EEG recovery following cerebral ischemia and reperfusion in the rat.

The efficacy of free radical scavengers (mannitol and n-2-mercaptopropionyl glycine) and a vasodilator (sodium nitroprusside) on the EEG recovery following cerebral ischemia was studied in the anesthetized rat. Global ischemia of brain was produced by the four-vessel occlusion for 30 min followed by 3 h reperfusion. Blood pressure, heart rate and EEG were monitored. The test agents were infused intravenously 15 min before and immediately after cerebral ischemia. The results indicate that mannitol 20-50 mg/kg, n-2-mercaptopropionyl glycine 10-20 mg/kg and sodium nitroprusside 20-50 micrograms/kg singly or in combination improved EEG recovery during reperfusion.

Animals↗
PubMed1990

Rapid verification of lambda-cDNA clones using mixed-base oligonucleotide as screening probe and sequencing primer.

A rapid procedure has been developed for the isolation and verification of cDNA clones isolated from a cDNA library based on lambda vectors. Using information of the partial amino acid sequence of a protein, synthetic mixed-base oligonucleotides are first employed as a screening probe using the plaque hybridization procedure. The cDNA inserts of the clones obtained are then directly amplified by polymerase chain reaction (PCR) using primers flanking the cloning site of the vector. Besides being used for cloning into a plasmid vector, the amplified DNA's are also subjected to nucleotide sequence analysis using the same mixed-base oligonucleotides as sequencing primers. This approach allows sequencing through the region of the known amino acid sequence for direct verification of the authenticity of the clones obtained. This procedure has successfully been used for cloning and partial characterization of the gene coding for a platelet aggregation inhibitor.

Amino Acid Sequence↗
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↗