Biomedical subjects

Q Z Zhang

Publications and source records attributed to Q Z Zhang.

17 recordsLinked to original sources

PubMed2001

Changes of oligosaccharides and fatty acids in monkey hippocampus by synaptic potentiation.

We measured the release of free fatty acids and structural changes of glycoprotein glycans induced by tetraethylammonium (TEA) salt in hippocampal slices of cynomolgus monkey brain. The release of free fatty acids in the hippocampal slices occurred after synaptic potentiation by TEA in a different manner from rat hippocampus. Arachidonic acid release in monkey hippocampus occurred much faster than that in rat. Several types of glycans of monkey hippocampal glycoproteins were determined depending on the duration time after TEA treatment. 5-Mannose was increased within 2 min, while polysialoglycans were increased after 5 min or later. Comparative study of glycans of monkey and rat hippocampal slices revealed the presence of relatively larger amount of sialo- and multi-anntenary glycans in rat than in monkey. These results indicate that the depolarizing stimulation of monkey hippocampal slices induced the change of glycoprotein glycan structures and release of free fatty acids in a different manner from rat hippocampus.

Animals↗

PubMed2001

Change of oligosaccharides of rat brain microsomes depending on dietary fatty acids and learning task.

We have analyzed oligosaccharide chains in brain microsomes of rats fed an n-3 polyunsaturated fatty acid-deficient (safflower oil group; S group) or -rich (perilla oil group; P group) diet before and after brightness-discrimination learning tasks. The amount of concanavalin A-binding sites (mainly mannoside) of the brain microsomes was found to be significantly less in the S group than the P group before the learning task. Detailed analysis of glycoprotein glycans demonstrated that high mannose type oligosaccharides were dominant in brain microsomes before the learning task in both dietary groups, whereas multiantennary complex-type oligosaccharides became dominant after the learning task and especially a tetra-antennary glycan, that had a core structure of the glycan of neural cell adhesion molecule, was more increased in the S-group than the P group. When polysialylated glycans were analyzed on serotonin-conjugated HPLC column, the glycans in the S-group microsomes before the learning task contained larger amount of higher affinity-polysialylated glycans to serotonin column than those in the P-group, and also contained larger amount of phosphoglycans that showed also high affinity to serotonin column than the P-group. Removal of mannoside from microsomes by alpha-mannosidase-treatment changed the membrane surface physical property, especially permittivity, as revealed by analysis of the interaction with 1-anilinonaphthalene-8-sulfonate. These results suggest that high mannose content and several multiantennary glycans including polysialylated and phospho-glycans were changed by dietary n-3 fatty acid deficiency and learning task in rat brain microsomal glycoproteins and that these changes may affect membrane functions through changes of membrane surface physical properties and reactivity against serotonin.

Animals↗

PubMed2001

Verapamil, cyproheptadine, and anisodamine antagonized [Ca2+]i elevation induced by TNFalpha in a single endothelial cell.

AIM: To study the effect of tumor necrosis factor alpha (TNFalpha) on intracellular free Ca2+ concentration ([Ca2+]i) and the effects of verapamil (Ver), cyproheptadine (Cyp), and anisodamine (Ani) on TNFalpha-induced [Ca2+]i changes in single endothelial cell, and to explore the mechanisms of TNFalpha-mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains (ECV304) were seeded in 35-mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca2+]i in single endothelial cell were determined by laser scanning confocal microscopy. RESULTS: After stimulation with TNFalpha, [Ca2+]i in single endothelial cell rapidly increased in a concentration-dependent manner and arrived at the peak value within 60 s, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca2+]i elevation was more obvious in nuclear than in cytoplasma and decreased slowly. Ver (1, 2 micromol/L), Cyp (30, 60 micromol/L), and Ani (20, 40 micromol/L) markedly inhibited TNFalpha 1.2 nmol/L-induced [Ca2+]i elevation. CONCLUSION: TNFalpha markedly induces elevation of [Ca2+]i in a single endothelial cell, it may be an important mechanism of TNFalpha-induced shock and tissue injury. That Cyp and Ani obviously suppress TNFalpha-induced [Ca2+]i elevation probably is one of the mechanisms of their antishock effects.

Biological Transport, Active↗

PubMed1999

Inhibitory effects of melatonin on free intracellular calcium in mouse brain cells.

AIM: To study the effects of melatonin (Mel) on cortical intrasynaptosomal calcium concentration in old mice and on [Ca2+]i elevation induced by Bay-K-8644, KCl, and sodium l-glutamate in isolated brain cells of neonatal mouse, and to determine the antiaging mechanism of Mel. METHODS: [Ca2+]i was measured in an RF-5000 recording spectrofluorophotometer by preloading the synaptosomes or cells with Fura 2-AM. RESULTS: Long term of administrating Mel inhibited the overload of [Ca2+]i in old mouse cerebral cortex. The [Ca2+]i in both high (20 mg.L-1) and low dose (1 mg.L-1) of Mel groups was reduced from (434 +/- 32) nmol. L-1 (the older control group) to (330 +/- 41) and (313 +/- 56) nmol.L-1, respectively, P < 0.01. Mel 0.01, 0.1, 1, and 3 mumol.L-1 remarkably reduced [Ca2+]i elevations in isolated newborn mouse brain cells induced by Bay-K-8644, KCl, and Glu. CONCLUSIONS: The inhibitory effect of Mel on neuronal [Ca2+]i overload is involved in its antiaging effect.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1999

Antagonistic effects of melatonin on glutamate release and neurotoxicity in cerebral cortex.

AIM: To observe the effects of melatonin (Mel) on glutamate (Glu) release from the cortical synaptosomes in old mice and on neurotoxicity induced by KCl, Glu in cultured cortical cells of fetal rat and to explore the antiaging mechanism of Mel. METHODS: Glu release by the synaptosomes in old mouse cerebral cortex was detected in a spectrofluorophotometer. The neuronal viability in primary cultures from rat cerebral cortex was assessed using MTT stain and lactate dehydrogenase (LDH) efflux in the bathing medium. RESULTS: Mel inhibited the K+ (30 mmol.L-1)-induced Glu release from synaptosomes either in calcium dependent or independent conditions [control (10.6 +/- 1.1), (9.2 +/- 0.7) mumol.g-1 (protein); Mel 0.1 mumol.L-1 (6.5 +/- 0.9), (7.5 +/- 0.6) mumol.g-1 (protein), respectively, P < 0.01 vs control group), increased MTT activity (control 0.67 +/- 0.04, 0.81 +/- 0.03; Mel 0.1 mumol.L-1 0.715 +/- 0.023, 0.925 +/- 0.027, P < 0.01 vs control group] and decreased LDH efflux (control 0.400 +/- 0.016, 0.379 +/- 0.016; Mel 0.1 mumol.L-1 0.345 +/- 0.021, 0.340 +/- 0.012, respectively, P < 0.01 vs control group), therefore, protected the neuronal viability against KCl and Glu-induced injury. CONCLUSION: The inhibitory effect of Mel on Glu release from cortical synaptosome and the protective effect of Mel on cortical neurons against neurotoxicity are its antiaging mechanisms.

Aging↗

PubMed1998

Quantification of concanavalin A binding to rat brain microsomal membranes detected by fluorescence polarization technique.

A high sensitive method for detecting the change of microsomal membrane surface oligosaccharides was developed to study the regulatory role of lipid- or peptide-linked mannoside of endoplasmic reticulum in synaptic functions. The binding of concanavalin A to the microsomal membrane surface was measured quantitatively using a microgram-order of rat brain microsomal proteins. The fluorescence polarization of concanavalin A (Con A)-fluorescein isothiocyanate (FITC) conjugate bound to the membrane was analyzed to quantitate the change of binding constant and the number of binding sites. As a control, the non-specific binding of bovine serum albumin-FITC conjugate was measured by the same technique. We measured the change of fluorescence intensity of membrane-bound FITC conjugates by the flow cytometry and found that the intensity of FITC conjugate bound to the membrane increased more than that of free form of the probe. We observed that the alpha-mannosidase-treatment of rat brain microsomes resulted in the increase of binding constant of Con A to the microsomal surface without significant loss of binding sites.

Animals↗

PubMed1994

[Genetic diagnosis of phenylketonuria. III. Mutations of phenylalanine hydroxylase gene in Orientals].

Phenylketonuria (PKU) is an autosomal recessive disorder caused by lesions in the phenylalanine hydroxylase (PAH) gene. The recent studies on PAH mutations show the genetic drift of PKU alleles among some Oriental populations. Therefore, we searched for PKU mutations among Japanese, Chinese and Taiwanese. Direct sequencing was conducted on DNA fragments amplified by the polymerase chain reaction, using solid-phase technology involving the biotin-streptavidin system. Two new mutations (R241C and G247V) and two of the known mutant alleles (Y204C and R243Q) were found in two Taiwanese and two Chinese PKU patients, and three known mutations (R111X, Y204C and R413P) were recognized in three Japanese; two new mutations were identified in exon 7 of the PAH gene at codon 241 and codon 247, where the single base changes from C to T and from G to T substituted cysteine for arginine and valine for glycine, respectively. Further all the PAH mutations detected are common in Oriental populations as they have been thus far unreported among Caucasians. From these data as well as the clinical phenotype of the patients, we suggest that the R241C and G247V substitutions may interfere with proper enzyme function, although we have not yet performed functional studies. More detailed studies would be needed to clarify the regional distribution of mutant chromosomes in Oriental populations and other unidentified mutations.

Alleles↗

PubMed1994

Effects of cyproheptadine on plasma superoxide dismutase activity and malondialdehyde content in rabbits with hemorrhagic shock.

Profound hemorrhagic shock was produced in thirty rabbits by exsanguination via the carotid artery until blood pressure (BP) reached 5.3 kPa (40 mmHg) and was sustained for a period of 90 minutes. The rabbits were equally divided into cyproheptadine (Cyp) treated group and control group. Blood samples 30 minutes after liquid and blood infusion and administration of Cyp (10 mg/kg) were collected from the carotid artery, and the plasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content measured. The results showed that Cyp remarkably enhanced the plasma SOD activity (2462 +/- 338 vs 1955 +/- 596, P < 0.01) and reduced MDA content (2.68 +/- 0.24 vs 3.20 +/- 0.49, P < 0.01). We believe that the increase of O2 production plays an important role in the development of shock, the single blood and liquid infusion can not significantly improve the shock conditions. Scavenging oxygen free radicals and alleviating cellular damage and multiple organ failure are the possible mechanisms of cyproheptadine anti-shock effect.

Animals↗

PubMed1994

Effects of cyproheptadine on TXB2 and 6-keto-PGF1 alpha plasma levels in rabbits with hemorrhagic shock.

Profound hemorrhagic shock was produced in 26 rabbits by exsanguination via carotid artery until blood pressure (BP) = 5.3 kPa (40 mmHg) for a period of 90 min. Rabbits were equally divided into a cyproheptadine (Cyp) treated group and a control group. The blood samples before and 90 min after shock and 30 min after liquid and blood infusion and administering Cyp (10 mg.kg-1) were collected from the carotid artery. With radioimmunoassay, we measured the thromboxane B2(TXB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) contents in plasma. The results indicated that the TXB2 and 6-keto-PGF1 alpha levels during shock (1024 +/- 924, 30 +/- 32) and after liquid and blood infusion (990 +/- 943, 60 +/- 54) were higher than those (221 +/- 134, 6 +/- 4) in normal rabbits (P < 0.01, P < 0.05). Cyp reduced obviously the TXA2 plasma level in rabbit with shock (304 +/- 299 vs 990 +/- 943, P < 0.05). We conclude that the decrease of TXB2 content is one of the possible mechanisms of cyproheptadine anti-shock effect.

6-Ketoprostaglandin F1 alpha↗

PubMed1992

Anti-shock effect of cyproheptadine in rabbit.

Twenty four New Zealand rabbits were equally divided into a cyproheptadine (Cyp) treated group and a control group. Profound hemorrhagic shock was produced by exsanguination via carotid artery until mean arterial pressure (MAP) = 5.3 kPa (40 mm Hg) for a period of 90 min. After given Cyp 10 mg.kg-1, the MAP and central venous pressure (CVP) of the treated group rose obviously (P less than 0.01) and the mesenteric microcirculation improved markedly. After 1 h, all indices returned nearly to the preshock state. The survival rate 2 h after Cyp increased to 12 (P less than 0.01) in comparison with the control group (7). The results showed that Cyp, which dilates the vasculature and improves the microcirculation through blocking serotonin S2 and histamine H1 receptors, has a beneficial anti-shock effect.

Animals↗

PubMed1987

Significance of the straight-leg-raising test in the diagnosis and clinical evaluation of lower lumbar intervertebral-disc protrusion.

The cases of 113 patients who had protrusion of a lumbar intervertebral disc were analyzed to determine the relationship between the findings at operation and the location of the pain that resulted from the straight-leg-raising test. The study showed a close relationship between the location of the pain and the position of the protrusion of the disc. The degree of limitation of straight-leg raising was also found to have a direct relationship to the size and position of the protrusion and to its relationship to the spinal nerve. The protrusions were classified into three types according to position in relation to the dura mater and to the pattern of pain that was induced by passive straight-leg raising. On straight-leg raising, central protrusions tended to cause pain in the back, lateral protrusions caused pain in the lower extremity, and intermediate protrusions caused both. On this basis, the distribution of pain on straight-leg raising allowed an accurate prediction of the location of the lesion in 100 (88.5 per cent) of the 113 patients.

Adolescent↗

PubMed1986