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Y T Huang

Publications and source records attributed to Y T Huang.

At least 19 recordsLinked to original sources
PubMed1998

Vascular hyporeactivity persists despite increased contractility after long-term administration of isosorbide dinitrate in portal hypertensive rats.

BACKGROUND/AIMS: Portal hypertension is associated with decreased vascular responsiveness to vasoconstrictors, which may contribute to the hyperdynamics. Isosorbide dinitrate is an effective portal hypotensive drug. The present study aimed to investigate whether chronic administration of isosorbide dinitrate could affect vascular responsiveness in portal hypertensive rats. METHODS: Portal hypertension was induced by partial portal vein ligation. Sham-operated (Sham) rats served as controls. There were four animal groups for this study: portal vein ligation-isosorbide dinitrate group, portal vein ligation-vehicle (Veh) group, Sham-isosorbide dinitrate group and Sham-Veh group. Isosorbide dinitrate (5 mg x kg(-1) x 12 h(-1) was given by gavage for 8 days starting 1 day before ligation and continuing thereafter. Mesenteric arteries were removed for contractile study after hemodynamic measurement. RESULTS: Contractile responses to KCI (15-90 mM) and phenylephrine (10(-9)-10(-4) M) were recorded. Both vascular reactivity and sensitivity were significantly reduced in portal vein ligation rats as compared to Sham rats. Chronic isosorbide dinitrate treatment reduced portal venous pressure in portal vein ligation rats. Moreover, the maximal contractile responses to KCl and phenylephrine were significantly enhanced in both portal vein ligation and Sham rats after isosorbide dinitrate treatment, but relative hyporeactivity persisted in portal vein ligation rats. In contrast, a single dose of isosorbide dinitrate did not alter the contractile sensitivity or reactivity to KCl or phenylephrine in either portal vein ligation or Sham rats. CONCLUSION: Our results show that long-term administration of isosorbide dinitrate enhanced vascular contractility in both portal vein ligation and Sham rats, but relative hyporeactivity persisted in portal vein ligation rats.

Administration, Oral↗
PubMed1998

Hemodynamic effects of eight-day octreotide and propranolol administration in portal hypertensive rats.

Octreotide and propranolol are both effective portal hypotensive drugs in the control or prevention of variceal bleeding. The present study was undertaken to investigate the hemodynamic effects of octreotide and propranolol, alone or in combination, in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation. Portal hypertensive rats were allocated into one of the four groups: vehicle group (saline, 0.5 ml/day), octreotide group (100 microg/kg/12 hr), propranolol group (30 mg/kg/day), and octreotide (100 microg/kg/12 hr) plus propranolol (30 mg/kg/day) group. Propranolol or saline was administered by gavage, octreotide by subcutaneous injection. Drug was given one day before ligation and continued for eight consecutive days. Systemic as well as splanchnic hemodynamic parameters were measured thereafter. The portal venous pressure, portal tributary blood flow, and cardiac index were significantly reduced by octreotide, propranolol, or octreotide plus propranolol in portal hypertensive rats. Portal territory, systemic, and renal vascular resistances were significantly enhanced, while hepatic arterial blood flow significantly reduced, in the octreotide and octreotide plus propranolol groups as compared to vehicle group. Our results showed that eight-day administration of octreotide, propranolol, or octreotide plus propranolol led to portal hypotensive and antihyperdynamic effects in portal hypertensive rats. Overall, octreotide treatment alone resulted in better antihyperdynamic profiles than propranolol treatment alone. The combination of octreotide and propranolol offered no therapeutic benefits and was slightly less effective than octreotide alone.

Adrenergic beta-Antagonists↗
PubMed1998

Haemodynamic effects of chronic octreotide and tetrandrine administration in portal hypertensive rats.

Octreotide is an effective portal hypotensive drug in the control of variceal bleeding. Tetrandrine is a type of calcium channel blocker recently reported to reduce portal hypertension. The present study was undertaken to investigate the haemodynamic effects of octreotide and tetrandrine, alone and in combination, in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation. Portal hypertensive rats were allocated into one of the four groups: vehicle group (saline, 0.5 mL/day), octreotide group (100 microg/kg per 12 h), tetrandrine group (20 mg/kg per 12 h), and octreotide (100 microg/kg per 12 h) plus tetrandrine (20mg/kg per 12 h) group. Tetrandrine or saline was administered by gavage, and octreotide by subcutaneous injection. The drug was given for 8 consecutive days, starting 1 day before ligation and continuing onwards. Haemodynamic parameters were measured thereafter, using the radioactive microsphere method. The portal venous pressure and portal tributary blood flow were significantly reduced, while portal territory and renal vascular resistances were significantly enhanced, by octreotide, tetrandrine, or octreotide plus tetrandrine in portal hypertensive rats, compared with the vehicle group. Our results showed that long-term administration of octreotide, tetrandrine, or octreotide plus tetrandrine led to portal hypotensive effects in portal hypertensive rats, but octreotide alone exerted better anti-hyperdynamic effects compared with tetrandrine alone. A combination of octreotide and tetrandrine offered no major beneficial anti-hyperdynamic effects compared with octreotide alone.

Alkaloids↗
PubMed1998

Portal hypotensive effects of DL-028 and prazosin on portal hypertensive rats.

The portal hypotensive effects of prazosin and DL-028 (chem- ical name: 3-[[4-(2-methoxyphenyl)piperazin-1-yl]methyl]- 2, 3-dihydroimidazo[1,2-c]quinazolin-5(6H)-one(27b)), a synthetic alpha1-adrenoceptor antagonist, were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Two weeks after ligation, when the hyperdynamic state was stabilized the rats were anesthetized after an overnight fast and cannulated for measuring mean arterial pressure (MAP), portal venous pressure (PVP), cardiac index (CI) and heart rate (HR). Both DL-028 and prazosin (1, 3.3 and 10 microgram/kg) induced dose-dependent decreases of PVP and MAP after intravenous infusion, with effects lasting for longer than 30 min. The maximum percentage reduction of PVP after DL-028 was 10, 10 and 15%, respectively, for the dosages given (1, 3.3 and 10 microgram/kg), and 5, 12 and 25%, respectively, after prazosin. CI was not changed by either drug. HR was not changed by either drug except DL-028 at 10.0 microgram/kg with a bradycardiac effect. Our results showed that both DL-028 and prazosin reduced PVP in portal hypertensive rats.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1998

Detection of transcripts initiated from two viral promoters (Cp and Wp) in Epstein-Barr virus-infected nasopharyngeal carcinoma cells and biopsies.

Different activation of Epstein-Barr virus (EBV) promoters results in distinct expression patterns of EBV nuclear antigens (EBNAs) and may further decide the role of EBV in the cellular pathogenesis. In EBV-associated nasopharyngeal carcinoma (NPC) biopsies, it has generally been believed that Q promoter (Qp)-initiated EBNA1 is the only EBNA gene to be expressed and that the other two viral promoters, Cp and Wp, which can lead to expression of EBNA1-6, are inactive. However, the failure to demonstrate the activities of Cp and Wp may have been due to the limited sensitivities of detection approaches used. In the present article, the EBV promoter usage and gene expression were re-examined in both EBV-infected NPC cells in vitro and NPC biopsies in vivo. An NPC cell line susceptible to EBV infection in vitro was established by transfection with a plasmid expressing a well-known EBV receptor, CR2. The presence of viral DNA and EBNA proteins was demonstrated in these EBV-infected cells using PCR and anticomplement immunofluorescence assay, respectively. As has been identified in NPC biopsies, viral transcripts of Qp-initiated EBNA1, latent membrane protein (LMP)1, LMP2A, LMP2B, and BamHI A genes, as well as the EBV-encoded small RNA (EBER)1 were detected in these in vitro-infected cells using reverse-transcription-PCR. Notably, viral transcripts initiated from Cp or Wp were also found in the infected cells. Furthermore, Cp- or Wp-initiated transcripts and EBNA2 mRNA were detected in some NPC biopsies. Taking advantage of this sensitive detection approach, our observation that Cp and Wp may be active in NPC cells raises the possibility that EBNA2 to 6, in addition to EBNA1, may play roles in the pathogenesis of NPC.

Adult↗
PubMed1997

Hemodynamic effects of chronic tetrandrine treatment in Sprague-Dawley rats.

Tetrandrine is a calcium channel antagonist with reported anti-hypertensive effect. The present study aimed to investigate the hemodynamic effects of chronic tetrandrine treatment on normotensive Sprague-Dawley rats. Animals were allocated into one of the two groups: tetrandrine group and vehicle group. Tetrandrine (20 mg/kg) or vehicle was administered by gavage every 12 hours for consecutive 8 days. After 8 days of tetrandrine treatment, systemic hemodynamics and organ blood flows were measured on the next morning after an overnight fast, using radioactive microsphere method. Mean arterial pressure (96 +/- 2 vs. 118 +/- 4 mmHg) and systemic vascular resistance (254 +/- 35 vs. 369 +/- 5 dyn.sec.cm5 x 10(3)/100 g body wt) were significantly decreased in the tetrandine group as compared to the vehicle group. The cardiac-index (35.2 +/- 2.7 vs. 25.5 +/- 0.8 mL/min/100 g body wt) was increased in the tetrandrine group. The portal venous pressure, portal tributary blood flow, portal territory vascular resistance, renal blood flow, renal vascular resistance, heart rate and body weight were similar between the two groups. In conclusion, long-term treatment of tetrandrine reduced mean arterial pressure and systemic vascular resistance but did not change splanchnic or renal hemodynamics in normal rats.

Alkaloids↗
PubMed1997

An aromatic stacking interaction between subunits helps mediate DNA sequence specificity: operator site discrimination by phage lambda cI repressor.

Sequence specific DNA binding by regulatory proteins provides the basis for regulation of initiation of transcription. A great deal of progress has been made toward understanding sequence specific recognition by individual protein subunits. An additional level of control that needs to be understood is that due to coupling between the subunits of oligomeric regulatory proteins. An example is the bacteriophage lambda cI repressor, a dimeric protein that regulates the lysogenic to lytic genetic switch of the phage. Two levels of specificity are critical to this regulation. First, like all transcriptional regulators, dimers distinguish operator from nonspecific DNA. Direct readout of the DNA sequence by the recognition helix is considered the well understood mechanism for this. However, differential affinity for O(R)1, O(R)2 and O(R)3 is equally critical to the switch because it mediates opposing regulation of divergent promoters. Site specificity at this second level is less well understood. Conformational adaptation by both the repressor and the different operators appears to be important. To evaluate how subunit-subunit interactions are involved in this process, we investigated the effects on both dimer stability and operator binding of amino acid substitutions at the contacts between the symmetrically related helices-5 in the dimer interface. Substitutions for Tyr88 alter dimer stability and greatly perturb differential operator affinity, but generally do not affect operator versus non-operator specificity. The pattern of these effects suggests that the geometry of the face-to-face aromatic stacking interaction between symmetrically related Tyr88 in each subunit, a group in the dimer interface but far removed from the DNA binding interface, plays a critical role in operator discrimination. Conformational changes in the tertiary structure of the subunits appears to be involved. By contrast, the significant effect of I84S substitution is to greatly decrease affinity for all three operators. Presumably, the altered packing of the dimer interface causes a quarternary structural change that moves the two helix-turn-helix motifs out of register with successive DNA major grooves.

Bacteriophage lambda↗
PubMed1997

Inositol phosphate responses in portal veins from portal hypertensive rats: receptor- and nonreceptor-mediated responses.

BACKGROUND/AIMS: Venous hyporesponsiveness in portal hypertension has been reported previously by us. The present study was undertaken to investigate possible changes of phosphoinositide signal transduction pathway in the portal veins from portal hypertensive rats METHODS: Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for measurement of [3H]inositol phosphate responses to both receptor- and nonreceptor-mediated stimuli. RESULTS: Basal [3H]inositol phosphate formation was similar between the two groups. Both phenylephrine and angiotensin II stimulated [3H]inositol phosphate formation in portal veins, but the responses were attenuated in the portal hypertensive group. In contrast, the [3H]inositol phosphate formation by nonreceptor-mediated stimuli (GTP gamma S, NaF/AlCl3, and phospholipase C) was similar between the two groups. CONCLUSION: Our results showed that the receptor-mediated [3H]inositol phosphate formation was attenuated, while the non-receptor-mediated formation was unaltered, in the portal vein from portal hypertensive rats.

Angiotensin II↗
PubMed1997

Selective cytotoxicity of ginkgetin from Selaginella moellendorffii.

Bioassay-directed fractionation of an ethanolic extract of Selaginella moellendorffii has led to the isolation of a known biflavone, ginkgetin (1). A dose-dependent inhibition was observed with 1 on the growth of OVCAR-3 (human ovarian adenocarcinoma) cells with 50% inhibition occurring at 1.8 micrograms/mL. Nonbioactive fractions yielded four additional known biflavones, amentoflavone 7,4',7",4"'-tetramethyl ether, kayaflavone, podocarpusflavone A, and amentoflavone.

Animals↗
PubMed1997

Evaluation of the quality of HLA antibodies in placental blood.

Two groups of blood samples, placental blood and female donor blood, were shown to have a frequency of 16.4 and 1.5% of anti-human leucocyte antigen (HLA) antibodies respectively. The specificities and qualities of these antibodies were further characterized by their relative coefficient (r) values and strength indices (SIs). Most had an r value of approximately one, but their SIs varied from 41 to 100%. Among these two groups, nine samples gave very strong and definite results (r = 1 and SI = 100%). Data analysis revealed that the qualities of the two groups were comparable. However, the antibody positive rate was higher in placental blood samples than that in donor blood samples.

Antibodies↗
PubMed1997

Chronic administration of propranolol improves vascular contractile responsiveness in portal hypertensive rats.

Propranolol is used clinically as a prophylactic drug to prevent oesophageal variceal bleeding in cirrhotic patients with portal hypertension. Vascular hyporesponsiveness is a common characteristic of the portal hypertensive state. The present study aimed to investigate whether chronic administration of propranolol could improve vascular responsiveness in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL). Sham-operated rats served as controls. There were four study groups: PVL-propranolol group (portal hypertensive rats receiving propranolol), PVL-vehicle group (portal hypertensive rats receiving saline), sham-propranolol group (sham-operated rats receiving propranolol) and sham-vehicle group (sham-operated rats receiving saline). Propranolol (30 mg kg-1 day-1) or saline was given for 9 days via gastric gavage starting 1 day before ligation and thereafter. Then, the superior mesenteric artery was removed from each group for contractile study after haemodynamic measurement. In portal hypertensive rats, propranolol significantly alleviated the hyperdynamic state, including portal pressure, cardiac index and total peripheral resistance in the treated group compared with the vehicle group. The maximal contractile responses to KCl and vasopressin in mesenteric artery were significantly greater in the sham-vehicle group than in the PVL-vehicle group. Long-term propranolol treatment enhanced the contractile reactivity of mesenteric artery to KCl and vasopressin in PVL rats, and the contractile profiles were corrected towards those in sham-treated animals. In contrast, propranolol treatment decreased heart rate, mean arterial pressure and cardiac index but did not alter the contractile responsiveness of sham-operated rats. These results showed that, in portal vein stenosed rats, long-term treatment with propranolol improved arterial contractile reactivity together with portal pressure reduction. The propranolol effect on vascular reactivity is probably related to haemodynamic improvement, instead of a direct contractile effect on the vasculature.

Animals↗
PubMed1997

Haemodynamic effects of chronic tetrandrine treatment in portal hypertensive rats.

Tetrandrine is a calcium channel antagonist with reported antihypertensive effect. However, the potential role of tetrandrine as a therapeutic agent in portal hypertension has yet to be explored. The present study aimed to investigate the haemodynamic effects of chronic tetrandrine treatment on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Animals were allocated into one of two groups: a tetrandrine group and a vehicle group. Tetrandrine (20 mg/kg) or vehicle was administered by gavage every 12 h for 8 consecutive days, starting 1 day before ligation and continuing thereafter. After 8 days of tetrandrine treatment, systemic haemodynamics, organ blood flow and the degree of portal-systemic shunting were measured after an overnight fast. The portal venous pressure and protal tributary blood flow were significantly decreased, while portal territory as well as hepto-collateral vascular resistance significantly increased in the tetrandrine group compared with the vehicle group. The cardiac index was increased, while systemic vascular resistance was decreased, the the tetrandrine group. Mean arterial pressure, heart rate, portal-systemic shunting and bodyweight were similar between the two groups. Renal blood flow was decreased in the tetrandrine group. In conclusion, long-term treatment of tetrandrine reduced portal venous pressure and alleviated splanchnic hyperaemina in portal hypertensive rats without affecting the portal-systemic shunting.

Alkaloids↗
PubMed1997

Portal hypotensive effects of tetrandrine and verapamil in portal hypertensive rats.

The portal hypotensive effects of tetrandrine and verapamil (both calcium-channel blockers) were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Both tetrandrine (4, 8, 16 and 24 mg kg-1) and verapamil (0.5, 1.0, 1.5 and 2.0 mg kg-1) induced dose-dependent decreases of portal venous pressure and mean arterial pressure after intravenous infusion. for example, infusion of tetrandrine (16 mg kg-1) induced a maximum reduction of portal venous pressure and mean arterial pressure approximately 1 min after the start of infusion. Portal venous pressure decreased from baseline (12.5 mmHg) to 10.0 mmHg, and mean arterial pressure from baseline (90 mmHg) to 80 mmHg. Heart rate decreased from 250 to 240 beats min-1. At 24 mg kg-1, tetrandrine reduced portal venous pressure and mean arterial pressure to 20.3 +/- 2.4% and 28.4 +/- 1.4% of baseline, respectively. Our results show that both tetrandrine and verapamil induce portal pressure reduction in portal hypertensive animals.

Alkaloids↗
PubMed1997

The hemodynamic effects of AT-112, an analog of ketanserin, in portal hypertensive rats.

A serotonin mechanism has been reported to contribute to the hyperdynamic circulation of portal hypertension. Different studies have demonstrated that serotonin antagonists decrease portal pressure in portal hypertensive patients and animals. The present study was undertaken to investigate the effect of AT-112, an analog of ketanserin, on portal hypertension induced by partial portal vein ligation in rats. Since ketanserin is known to possess alpha 1-adrenergic antagonistic activity, the effect of AT-112 was compared to that of prazosin. A single dose (prazosin 4.2 micrograms/kg, AT-112 1 mg/kg) was chosen to produce a similar hypotensive effect (-20 +/- 4% for prazosin and -24 +/- 4% for AT-112). At this dose, prazosin significantly decreased total peripheral resistance whereas AT-112 significantly decreased cardiac index and heart rate. Both agents significantly decreased the portal tributary blood flow and portal pressure. In rats receiving AT-112, a significant correlation was found between the magnitudes of decrease in cardiac index and the decrease in portal tributary blood flow. We also found that the magnitude of reduction in portal pressure was greater following AT-112 administration. This study suggested that AT-112 may have more beneficial hemodynamic effects than prazosin in portal hypertensive rats. Our results provide further support for the serotonergic mechanism in the pathogenesis of hyperdynamic circulation in portal hypertension.

Animals↗
PubMed1997

Hemodynamic effects of chronic tetrandrine and propranolol administration on portal hypertensive rats.

The purpose of this study was to investigate the therapeutic effects of tetrandrine and propranolol, alone or in combination, on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Animals were allocated into one of the four groups: vehicle group (0.1 N.HCl, 0.7 ml/day), tetrandrine group (50 mg/kg/ day), propranolol group (30 mg/kg/day), and tetrandrine (50 mg/kg/day) plus propranolol (30 mg/kg/day) group. Drug or vehicle was administered by gavage for consecutive 9 days. After 9 days of treatment, the portal venous pressure and mean arterial pressure in each treatment group were significantly lower than those in the vehicle group. The cardiac index was not changed by tetrandrine alone, but reduced in the two groups receiving propranolol alone or in combination. Total peripheral resistance was significantly decreased in the tetrandrine group and significantly increased in the tetrandrine plus propranolol group as compared with the vehicle group. Our results suggested that tetrandrine or propranolol alone induced portal hypotensive effects, with propranolol achieving better antihyperdynamic effects in terms of cardiac index, and in combination propranolol effects predominated over those of tetrandrine.

Administration, Oral↗
PubMed1997

Suppression of protein kinase C and nuclear oncogene expression as possible molecular mechanisms of cancer chemoprevention by apigenin and curcumin.

Apigenin, a less-toxic and non-mutagenic flavonoid, suppressed 12-0-tetradecanoyl-phorbol-13-acetate-(TPA)-mediated tumor promotion of mouse skin. TPA had the ability to activate protein kinase C (PKC) and induced nuclear proto-oncogene expression. Our study indicates that apigenin inhibited PKC by competing with adenosine triphosphate (ATP). Apigenin also reduced the level of TPA-stimulated phosphorylation of cellular proteins and inhibited TPA-induced c-jun and c-fos expression. Curcumin, a dietary pigment phytopolyphenol, is also a potent inhibitor of tumor promotion induced by TPA in mouse skin. When mouse fibroblast cells were treated with TPA alone, PKC translocated from the cytosolic fraction to the particulate fraction. Treatment with 15 or 20 microM curcumin for 15 min inhibited TPA-induced PKC activity in the particulate fraction by 26-60%. Curcumin also inhibited PKC activity in vitro by competing with phosphatidylserine. Curcumin (10 microM) suppressed the expression of c-jun in TPA-treated cells. Fifteen flavonoids were examined for their effects on morphological changes in soft agar and cellular growth in v-H-ras transformed NIH3T3 cells. The results demonstrated that only apigenin, kaempferol, and genistein exhibited the reverting effect on the transformed morphology of these cells. Based on these findings, it is suggested that the suppression of PKC activity and nuclear oncogene expression might contribute to the molecular mechanisms of inhibition of TPA-induced tumor promotion by apigenin and curcumin.

Animals↗
PubMed1996

Effects of long-term administration of octreotide in portal vein-stenosed rats.

The hemodynamic effects of long-term administration of octreotide in portal hypertension has not been established. In addition, whether long-term octreotide treatment prevents the development of portosystemic shunts has not yet been evaluated. Hence, the current study was undertaken to evaluate the effects of long-term administration of octreotide in rats with portal vein stenosis. Immediately after portal vein stenosis or sham operation, rats were given either a long-term octreotide administration of 100 micrograms/kg or a placebo every 12 hours by subcutaneous injection for 14 consecutive days. Systemic hemodynamics and regional blood flows, degree of mesenteric-systemic shunts, and plasma glucagon concentrations were measured after the final dose of octreotide or placebo. A fifth group of portal vein-stenosed rats received hemodynamic and plasma glucagon measurements after 1-day octreotide treatment given at 14 days after surgery. Long-term octreotide treatment modified the hyperdynamic circulation without affecting the degree of mesenteric-systemic shunts, and 1-day octreotide treatment decreased portal tributary blood flow without affecting the portal pressure, systemic hemodynamics, and degree of mesenteric-systemic shunts. Plasma glucagon levels were decreased in portal vein-stenosed rats receiving either long-term or 1-day octreodtide compared with rats receiving placebo. In contrast, chronic octreotide treatment did not affect any of the hemodynamic values or plasma glucagon levels in sham-operated rats. In conclusion, long-term administration of octreotide modified in part the development of portal hypertension and hyperdynamic circulation in portal vein-stenosed rats without affecting the degree of mesenteric-systemic shunts.

Analysis of Variance↗