Biomedical subjects

G Q Zeng

Publications and source records attributed to G Q Zeng.

30 records · Page 2Linked to original sources

PubMed1993

Platelet activating factor production in bovine cerebral microvascular endothelial cells and its drug inhibition.

The production of platelet activating factor (PAF) in bovine cerebral microvascular endothelial cells (CME cells) and the effects of tetrandrine (Tet) and dauricine (Dau) on the PAF production were investigated. PAF was determined by the aggregation of washed rabbit platelets. The results showed that the CME cells produced PAF 5.93 ng/8.5x 10(5) cells under the calcimycin 2.5 mumol.L-1 stimulation. Tet and Dau 1, 10, and 100 mumol.L-1 inhibited the production of PAF by 18.2%, 51.8%, 56.8%, and 26.3%, 63.3%, 65.9%, respectively. Tet concentration-dependently inhibited the PAF 9.1 nmol.L-1 induced washed rabbit platelets aggregation with the IC50 of 3.05 mumol.L-1 (95% confidence limits: 0.59-15.86 mumol.L-1). The binding of [3H]triazolodiazepine to the CME cells was partially displaced by Tet 0.02-33.00 mumol.L-1. It is suggested that the cerebrovascular system produces PAF at the pathological conditions and the inhibition of Tet and Dau.

Alkaloids↗

PubMed1992

[Effects of platelet activating factor on the cerebrovascular permeability in rats and the protection by drug].

The action of platelet activating factor in the rat brain was detected by Evans blue staining after injection of PAF into the rat brain. The results show that PAF increased the Evans blue staining of the brain, but no staining was observed without prior injection of PAF. Meanwhile, PAF was shown to stimulate the release of 14C-arachidonic acid (14C-AA) in the cerebral microvascular smooth muscle cells (CMSMC). SZ-1, a new synthetic drug, dose-dependently inhibited the Evans blue staining of the rat brain and the PAF induced 14C-AA release in CMSMC. These results indicate that the action of PAF in the rat brain might be related to the stimulation of AA release. SZ-1 may antagonize the PAF receptor and protect the brain from PAF induced damage.

Animals↗

PubMed1992

Specific binding sites of platelet activating factor on the intact bovine cerebral microvascular endothelial cells and antagonism of drugs.

[3H]Triazolodiazepine ([3H]WEB 2086), an antagonist of platelet activating factor (PAF) receptor, was studied as radioligand on intact cerebral microvascular endothelial cells (CMEC). The results showed that the binding of [3H]triazolodiazepine reached and maintained at an equilibrium after 15-120 min of incubation and that it was saturable with increasing concentration of radioligand. Scatchard analysis indicated that there were 2 specific binding sites on CMEC, its Kd1, Bmax1, Kd2, and Bmax2 were 3.13 nmol.L-1, 1.50 pmol/3 x 10(5) cells, 83.96 nmol.L-1, and 12.96 pmol/3 x 10(5) cells, respectively. The binding of [3H]triazolodiazepine to CMEC was displaced by C16-PAF and 1,5-bis-(3,4-dimethoxyphenyl)-tetrahydro-(4H)-pyran (SZ-1), which IC50 were 0.43 nmol.L-1 and 0.125 mumol.L-1, respectively. These data suggested the existence of PAF specific binding sites on CMEC.

Animals↗

PubMed1992

Effects of dauricine and anisodamine on LTs and PAF induced DNA synthesis in bovine anterior cerebral arterial smooth muscle cells.

The effects of leukotrienes (LTs) and platelet activating factor (PAF) on DNA synthesis in bovine anterior cerebral arterial smooth muscle cells were studied. The results showed that LTB4, LTD4 and PAF were all stimulatory to the cells. The maximal rates of stimulation were 32%, 29% and 77%, respectively, for LTB4, LTD4 and PAF at 10(-7) mol/L. Both dauricine and anisodamine at concentrations of 10(-7) to 10(-4) mol/L exhibited strong inhibitory effects on LTs and PAF induced DNA synthesis.

Alkaloids↗

PubMed1992

Leukotriene C4 receptors in cultured smooth muscle cells from bovine anterior cerebral arteries and microcerebrovasculatures.

Specific receptors for leukotriene C4 (LTC4) were identified on smooth muscle cells isolated from bovine anterior cerebral arteries (BACASMC) and bovine microcerebrovasculatures (BMSMC). [3H]LTC4 specific bindings to both cells at a fixed input reached the maxima at 60 min and 20 min, respectively. With incremental inputs of radioligand and a constant cell number, [3H]LTC4 specific bindings reached a plateau indicative of a saturable binding site. Analysis of Scatchard plots demonstrated a single population of high-affinity binding sites in both cells. The dissociation constant (Kd) for BACASMC was 39.2 +/- 1.3 nmol.L-1 and its Bmax was 19.3 +/- 2.1 pmol/10(6) cells. For BMSMC, Kd = 2.0 +/- 0.4 nmol.L-1, Bmax = 157 +/- 13 fmol/10(6) cells. The specific [3H]LTC4 bindings was inhibited by unlabeled LTC4, LTD4 and FPL-55712 (an SRS-A antagonist). The inhibitory rates for BACASMC were 70.4% and 35.3% by LTC4 and FPL-55712 at 1 mumol.L-1, respectively. For BMSMC the inhibitory rates were 96.9%, 73.9%, and 44.9% by LTC4, LTD4, and FPL-55712 at 10 mumol.L-1, respectively.

Animals↗

PubMed1991

Effects of anisodamine and dauricine on proliferation, DNA synthesis, and calcium influx in bovine anterior cerebral arterial smooth muscle cells in culture.

The in vitro culture of bovine anterior cerebral arterial smooth muscle cells (BACASMC) was first established in our laboratory. Anisodamine and dauricine inhibited the proliferation, DNA synthesis and calcium influx in the cells in dose-dependent manners. At 0.01 mmol.L-1, both drugs inhibited the proliferation by 17.6% and 8.3%, the DNA synthesis by 11.9% and 56.8%, the calcium influx by 26.6% and 31.4%, respectively. The results indicated that anisodamine and dauricine might have prospect in the prevention and treatment of cerebrovascular diseases.

Alkaloids↗

PubMed1990

Cyclic AMP synthesis in Escherichia coli strains bearing known deletions in the pts phosphotransferase operon.

A series of isogenic strains harboring known deletions in the pts operon of Escherichia coli have been constructed by reverse genetics. Strains bearing deletions for the whole pts operon failed to grow on maltose or on carbon sources of the same class. In these strains the total cAMP synthesis was significantly lower than in a strain deleted only for the crr gene. This indicated that enzyme I or phosphorylated histidine-containing phosphotransferase protein in addition to its role in phosphorylating enzyme IIIGlc, is involved in adenylate cyclase (AC) activation or cAMP excretion. It was further shown that deletions in the pts operon do not affect synthesis of AC.

Adenylyl Cyclases↗

PubMed1990

[Inhibitory effect of dauricine on platelet activating factor released from calcimycin-induced mouse peritoneal macrophages].

The effects of dauricine (Dau) on the release of platelet activating factor (PAF) from mouse peritoneal macrophages stimulated by calcimycin (A-23187) was studied. The method of sodium [3H]acetate incorporating into macrophages to synthesize PAF was set up for the first time. Calcimycin (0.2 mumol/L) significantly induced mouse peritoneal macrophages to utilize sodium [3H]acetate to synthesize PAF. PAF released from macrophages medium fluid increased as the concentration of sodium [3H]acetate increased. The maximal amount of PAF released from macrophages was attained by incubating macrophages with sodium [3H]acetate (250 mumol/L) and calcimycin (2 mumol/L) over 30 min. Extracted by CHCl3:CH3OH:H2O (2:2:1.8), separated by thin layer chromatography (TLC) and determined by liquid scintillation counting, PAF released was inhibited significantly by Dau both in time (10-30 min) and dose (1-1000 mumol/L) dependent manners. The IC50 of Dau for the formation of PAF was 2.5 mumol/L. On the same condition PAF release was also significantly inhibited by quinacrine at 500 mumol/L. The results indicate that Dau is a potent inhibitor of PAF synthesis in mouse peritoneal macrophages.

Alkaloids↗

PubMed1990

[Effects of silybin on production of oxygen free radical, lipoperoxide and leukotrienes in brain following ischemia and reperfusion].

Brain ischemia was produced by occluding bilateral common carotid arteries of Mongolia gerbil with clips for 30-min and reperfusion was established by removing the clips. Superoxide dismutase (SOD) in brain tissue was measured by chemoluminescence, malondialdehyde (MDA) by fluorescence spectrometry and leukotrienes (LT) by bioassay. Decrease of SOD and increase of MDA were significant in the brain after 30-min ischemia followed by 2-min reperfusion; The level of SOD increased from 13.4 +/- 2.7 to 18.8 +/- 3.0, 19.8 +/- 2.5, 22.1 +/- 3.9 x 10(3) units/g brain tissue and MDA decreased from 218 +/- 26 to 169 +/- 41, 167 +/- 36, 167 +/- 44 nmol/g brain tissue respectively by ip silybin 100, 200 and 400 mg/kg 30-min before occlusion. LT decreased from 3.1 +/- 1.0 to 1.5 +/- 0.4 ng/g brain tissue after ip silybin 200 mg/kg. It suggested that the protective effect of silybin on ischemic brain result from the inhibition of 5-lipoxygenase and lipoperoxide and scavenging of oxygen free radical.

Animals↗

PubMed1990

[Inhibitory effects of dauricine and anisodamine on production of prostaglandins on bovine cerebral arterial smooth muscle cells].

The effects of dauricine (Dau), aniso amine (Ani), platelet activating factor (PAF), leukotriene C4 (LTC4) and leukotriene D4 (LTD4) on the production of TXB2 and 6-keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2, respectively) in bovine anterior cerebral arterial smooth muscle cells were studied. The normal quantities of TXB2 and 6-keto-PGF1 alpha produced by bovine anterior cerebral arterial smooth muscle cells were 16 +/- 5 and 464 +/- 24 pg/10(5) cells, respectively, when measured by radioimmunoassay (RIA). The levels of TXB2 and 6-keto-PGF1 alpha in bovine anterior cerebral arterial smooth muscle cells decreased significantly when the cells were treated with Dau or Ani over 20 min. Both drugs inhibited the production of TXB2 and 6-keto-PGF1 alpha in dose (1-100 mumol/L) dependent manner. The bovine anterior cerebral arterial smooth muscle cells were stimulated markedly by LTC4 and LTD4 to produce TXB2 and 6-keto-PGF1 alpha on the same condition even at 0.01 mumol/L. When the cells were treated with PAF over 20 min, TXB2 increased significantly, but 6-keto-PGF1 alpha remained unchanged. If the cells were preincubated with Dau or Ani 20 min before PAF, LTC4 or LTD4 stimulation, the production of TXB2 and 6-keto-PGF1 alpha especially TXB2 were inhibited significantly compared with that of PAF, LTC4 or LTD4 group, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1985

Hormone concentrations before and after semen-induced ovulation in the bactrian camel (Camelus bactrianus).

During the follicular phase of bactrian camels, basal concentrations of LH were 2.7 +/- 1.2 ng/ml. By 4 h after insemination peak values of 6.9 +/- 1.0 ng/ml occurred. In addition, a smaller LH peak (5.4 +/- 2.5 ng/ml) appeared 1 day before regression of the follicle began in unmated camels. During the follicular phase peripheral plasma progesterone values were low (0.36 +/- 0.28 ng/ml), but values increased to reach 1.73 +/- 0.74 ng/ml at 3 days and 2.4 +/- 0.86 ng/ml at 7 days after ovulation. Plasma oestradiol-17 beta concentrations were 26.8 +/- 9.0 pg/ml during the follicular phase and 30.8 +/- 5.1 pg/ml when the follicle was maximum size. Values fell after ovulation but rose to 29.8 +/- 6.5 pg/ml 3 days later.

Animals↗

PubMedDate not supplied

Mutational analysis of the enzyme IIIGlc of the phosphoenolpyruvate phosphotransferase system in Escherichia coli.

The phosphoenolpyruvate phosphotransferase system (PTS) component EIIIGlc is responsible for transport and phosphorylation of glucose via EIIGlc. It also regulates the catabolism of other carbon sources, such as lactose and maltose, by modulating both the intracellular concentrations of the corresponding inducers and of cAMP. Mutational analysis of EIIIGlc was performed in order to identify crucial residues mediating the interactions between EIIIGlc and its target proteins. Such mutations were isolated by in vitro hydroxylamine mutagenesis of the cloned EIIIGlc gene, crr. Five mutated EIIIGlc impaired in the function of inducer exclusion were obtained. However, these mutations did not abolish the function of EIIIGlc in the transport and phosphorylation of glucose, nor in activation of adenylate cyclase. A single amino acid change was found for each mutation, which is located in a restricted area of the polypeptide chain: Gly47-->Ser47 for the HA2 and HA5 mutations, Ala76-->Thr76 for HA4 mutation and Ser78-->Phe78 for HA3 mutation, indicative of quaternary interactions between the corresponding region of EIIIGlc and its target protein(s).

Adenylyl Cyclases↗