Biomedical subjects

Wei-Ping Zhang

Publications and source records attributed to Wei-Ping Zhang.

At least 37 records · Page 2Linked to original sources

PubMed2005

Protective effects of baicalin on oxygen/glucose deprivation- and NMDA-induced injuries in rat hippocampal slices.

Baicalin is a flavonoid derivative from Scutellaria baicalensis Georgi with various pharmacological effects. Recently, the neuroprotective effect of baicalin was reported. To confirm this effect and explore the possible mechanism, we have investigated the protective effect of baicalin on ischaemiclike or excitotoxic injury and the activation of protein kinase C alpha (PKC(alpha)) in rat hippocampal slices. In-vitro ischaemic-like injury was induced by oxygen/glucose deprivation (OGD) and the excitotoxic injury by N-methyl-D-aspartate (NMDA). The viability and swelling of the slices were detected by triphenyltetrazolium chloride (TTC) staining and image analysis of light transmittance (LT), respectively. The translocation of PKC(alpha) was measured by immunoblotting. Baicalin was added during both injuries. Baicalin (0.1, 1, and 10 micromol L(-1)) concentration-dependently inhibited OGD-induced viability reduction and acute neuron swelling, and inhibited the increased portion of PKC(alpha) present in the membrane fraction over the total PKC(alpha). Baicalin ameliorated NMDA-induced viability reduction (not LT elevation) and inhibited the NMDA-increased membrane portion of PKC(alpha) at 1 micromol L(-1). We concluded that baicalin had a protective effect on ischaemic-like or excitotoxic injury in rat hippocampal slices, which might have been partly related to inhibition of PKC(alpha) translocation.

Animals↗

PubMed2005

[Expression of bFGF and VEGF in acute leukemia and its effects on HL-60 cell growth].

The study was to investigate the expression levels of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in the serum of patients with acute leukemia and supernatants of leukemia cell lines as well as effects of VEGF-specific antisense oligodeoxynucleotides (ASODN) on the growth of HL-60 cells. Meanwhile the methods to evaluate the VEGF level in the serum of patients with acute leukemia were explored. The levels of bFGF and VEGF in the serum from 32 patients with acute leukemia and 10 healthy subjects and in the supernatants of 5 various human leukemia cell lines were quantified by means of the enzyme-linked immunosorbent assay (ELISA) and were compared. VEGF levels were evaluated not only without standardization but also after standardized by platelet and finally expressed as VEGF/PLT (pg/10(6)). After with different concentrations of VEGF ASODN, HL-60 cell viability was examined with MTT assay and VEGF levels in supernatants were measured with ELISA, respectively. The results showed that bFGF was detected (3 pg/ml) in 14 out of 32 serum samples from patients with acute leukemia, and the positive (37.5%) was significantly higher than that in healthy controls (10%) (P < 0.01). 3 out of 5 supernanant samples obtained from leukemia cell lines demonstrated positive for bFGF as well. There is no difference of the serum VEGF levels between leukemia patients and healthy controls, but the serum VEGF levels in the serum from leukemia patients were significantly higher than those in healthy controls (P < 0.05) after standardization. 4 out of 5 leukemia cell (U937 excluded) were found to express VEGF in the supernanant. After exposure of HL-60 cells to VEGF ASODN at a concentration of 0.5, 1 and 5 micromol/L for 24 hours, the cell viability gradually dropped down to lower levels (P < 0.05 vs controls). After treatment of HL-60 cells with VEGF ASODN at a concentration of 1, 5 and 20 micromol/L for 24 hours, the VEGF levels in supernatants of target cells decreased (P < 0.05 vs controls). The patients with acute leukemia represented the higher levels of serum bFGF and VEGF than controls. Most of leukemia cell lines expressed bFGF and VEGF at different levels. It is concluded that bFGF and VEGF both have effects on regulations of angiogenesis in acute leukemia, but VEGF plays a pivotal role. VEGF-specific ASODN may have a role in them VEGF expression downregulated. Different results may be obtained in the evaluation of VEGF levels in the serum of patients with acute leukemia if different calculation methods are used. The methods reported can measure leukemia associated VEGF more accurately.

Acute Disease↗

PubMed2005

[Effect of bone marrow stromal cells on the apoptotic sensitivity of HL-60 and HL-60/VCR cells].

This study was aimed to investigate the effects of human bone marrow fibroblastoid stromal cell line (HFCL) on chemosensitivity of acute myeloid leukemia sensitive HL-60 cell line and multidrug-resistant (MDR) HL-60/VCR cell line in vitro co-culture. Setting up co-culture system of HL-60 or HL-60/VCR cells in direct contact with HFCL cells, or with HFCL cells separated by transwell, and exposing HL-60 or HL-60/VCR cells to different concentrations of topotecon (TPT), morphologic evidence for apoptosis was determined by staining with Wright-Giemsa stain and acridine orange/ethidium bromide (AO/EB). Cell cycle, sub-G(1) and annexin V FITC staining were detected by flow cytometry. The expression of active caspase-3, Bcl-2 and Pgp was detected by Western blot. The results showed that HL-60 or HL-60/VCR cells treated by TPT revealed characteristic apoptotic morphological changes by Wright-Giemsa and AO/EB staining. The percentage of annexin V-positive cells and apoptotic cells decreased when they were cocultured with HFCL cells. The proportion of G(0)/G(1) HL-60 or HL-60/VCR cells treated by TPT increased and the sub-G(1) appeared significantly, but apoptotic and sub-G cells reduced after direct contact with HFCL cells. Meanwhile, although HL-60 or HL-60/VCR cells treated by TPT expressed activated caspase-3, and the expression of Bcl-2 decreased, the expression of activated caspase-3 decreased and Bcl-2 increased after direct contact with HFCL cells. In conclusion, HFCL stromal cells can prevent TPT-induced apoptosis in HL-60 and HL-60/VCR cells via modulation of Bcl-2 and active caspase-3.

Antineoplastic Agents↗

PubMed2005

[Relationship of the disturbed balance between matrix metalloproteinases and their tissue inhibitors and the invasion of malignant salivary gland tumours].

OBJECTIVE: To detect protein expression of MMPs and TIMPs in various salivary gland neoplasms and to investigate their roles in invasion and metastasis of the malignant salivary gland tumors. METHODS: Immunohistochemistry and Gelatin zymography analyses for MMP-2, MMP-9, MT1-MMP, TIMP-1 and TIMP-2 were performed in 26 malignant and 28 benign salivary gland tumors. RESULTS: The expression of MMP-2 and MMP-9 was significantly higher in carcinomas than in adenomas (P < 0.05). The MMP-2/TIMP-1 and MMP-2/TIMP-2 was also significantly higher in carcinomas than in adenomas (P < 0.05). There was a cooperated effect among MMP-2, MT1-MMP and TIMP-2. The expression of active MMP-2, proMMP-9 and active MMP-9 was significantly higher in malignant tumors than in benign tumors (P < 0.05). CONCLUSION: MMP-2 and MMP-9 may play important roles in invasion of malignant salivary gland tumors. A disturbed balance between MMP-2, MMP-9, TIMP-1 and TIMP-2 in malignant salivary gland tumors was detected. It was the absolute increase of MMP-2 and MMP-9 to induce the unbalance.

Enzyme Precursors↗

PubMed2005

[Recipient lymphopenia state enhances the expansion and anti-leukemia effect of leukemia specific cytotoxic T lymphocytes].

OBJECTIVE: To determine the role of recipient lymphopenia state in the expansion and function of leukemia specific cytotoxic T lymphocytes (CTLs). METHODS: C57BL/6 mice were induced to lymphopenia with 6 Gy total body irradiation. Spleen T cells or leukemia specific T cells from EGFP+ transgenic C57BL/6-EGFP mice were adoptively transferred by intravenous injection. The mice were challenged subcutaneously with 1 x 10(6) FBL3 leukemic cells at day 2 after irradiation. The peripheral WBC count, percentage of EGFP+ cells, subsets of T cells and tumor sizes were monitored. RESULT: Both of the spleen T cell and leukemia specific CTL proliferated efficiently with the percentage of EGFP+ cells of 28. 81% and 42.24%, respectively, after infused into lymphopenic recipients. However, spleen T cells had no anti-leukemia effect regardless of its expansion. In contrast, leukemia specific CTLs showed a more rapid and extensive expansion under the condition of lymphopenia and a enhanced anti-leukemia immunity. CONCLUSION: Transfusion of leukemia specific CTLs under lymphopenia state could be a feasible strategy to expand leukemia specific CTLs and generate favorable anti-leukemia effect in vivo.

Animals↗

PubMed2004

Minocycline protects PC12 cells from ischemic-like injury and inhibits 5-lipoxygenase activation.

Minocycline protects animals against cerebral ischemia by inhibiting inflammation. To determine whether minocycline protects PC12 cells from in vitro ischemic-like injury and affects pro-inflammatory 5-lipoxygenase activation, the cell viability and 5-lipoxygenase translocation to nuclear membrane were observed after oxygen-glucose deprivation (OGD). We found that OGD reduced cell viability, which was attenuated by minocycline and 5-lipoxygenase inhibitor caffeic acid. 5-Lipoxygenase protein was detected in PC12 cells by immunohistochemical and Western blot analyses. OGD induced 5-lipoxygenase translocation to nuclear membranes, which was abolished by minocycline and caffeic acid. Thus, minocycline can protect PC12 cells from in vitro ischemic-like injury, and this effect may be partly related to the inhibition of 5-lipoxygenase activation.

Animals↗

PubMed2004

Montelukast, a cysteinyl leukotriene receptor-1 antagonist, dose- and time-dependently protects against focal cerebral ischemia in mice.

Our previous studies showed that cysteinyl leukotriene receptor-1 (CysLT1) antagonist pranlukast has a neuroprotective effect on cerebral ischemia in rats and mice. However, whether the neuroprotective effect of pranlukast is its special action or a common action of CysLT1 receptor antagonists remains to be clarified. This study was performed to determine whether montelukast, another CysLT1 receptor antagonist, has the neuroprotective effect on focal cerebral ischemia in mice, and to observe its dose- and time-dependent properties. Permanent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Montelukast was injected intraperitoneally either as multiple doses (once a day for 3 days and 30 min before MCAO) or as a single dose (at 30 min before, 30 min after, or 1 h after MCAO), respectively, and pranlukast and edaravone were used as controls. The neurological deficits, infarct volumes, brain edema, neuron density, and Evans blue extravasation in the brain were determined 24 h after MCAO. Pretreatments with multiple doses or a single dose of montelukast (0.1 and 1.0 mg/kg) before MCAO significantly attenuated all the ischemic insults. Post-treatment with a single dose of montelukast (0.1 and 1.0 mg/kg) at 30 min after MCAO also significantly decreased brain edema and infarct volume, but not neurological deficits. However, post-treatment with a single dose of montelukast at 1 h after MCAO had no significant effect. Pranlukast showed the same effects as montelukast, but edaravone attenuated the ischemic insults only with multiple doses before MCAO. Thus, montelukast has a dose- and time-dependent neuroprotective effect on permanent focal cerebral ischemia in mice, with an effective dose range of 0.1-1.0 mg/kg and a therapeutic window of 30 min. These findings further support the therapeutic potential of CysLT1 receptor antagonists in the treatment of cerebral ischemia at earlier phases.

Acetates↗

PubMed2004

Expression of cysteinyl leukotriene receptor 1 in human traumatic brain injury and brain tumors.

Cysteinyl leukotrienes (CysLTs) are potent proinflammatory mediators. CysLT receptor 1 (CysLT(1)) is one of the two CysLT receptors that has been cloned. Although the expression of CysLT(1) in the brain has been demonstrated by Northern blot and RT-PCR analyses, the location of CysLT(1) in the brain remains unknown. The objective of this study was to examine the distribution of CysLT(1) by immunohistochemical analysis in human brains with traumatic injury or tumors. CysLT(1) was expressed intensely in the microvascular endothelial cells in both normal and abnormal conditions. At 8 days after traumatic injury, microvascular regeneration was found and all of the endothelial cells highly expressed CysLT(1). In gray and white matters of the normal regions of the brain, CysLT(1) was expressed weekly or not at all. However, the CysLT(1) expression increased in the neuron- and glial-appearing cells in gray and white matters after traumatic brain injury. CysLT(1) was also detected in astrocytoma, ganglioglioma and metastatic adenocarcinoma, and the expression in the neuron- and glial-appearing cells around brain tumors increased robustly.

Adult↗

PubMed2004

A distinct role for norepinephrine in memory retrieval.

A role for norepinephrine in learning and memory has been elusive and controversial. A longstanding hypothesis states that the adrenergic nervous system mediates enhanced memory consolidation of emotional events. We tested this hypothesis in several learning tasks using mutant mice conditionally lacking norepinephrine and epinephrine, as well as control mice and rats treated with adrenergic receptor agonists and antagonists. We find that adrenergic signaling is critical for the retrieval of intermediate-term contextual and spatial memories, but is not necessary for the retrieval or consolidation of emotional memories in general. The role of norepinephrine in retrieval requires signaling through the beta(1)-adrenergic receptor in the hippocampus. The results demonstrate that mechanisms of memory retrieval can vary over time and can be different from those required for acquisition or consolidation. These findings may be relevant to symptoms in several neuropsychiatric disorders as well as the treatment of cardiac failure with beta blockers.

Adrenergic Agonists↗

PubMed2004

Potency of catecholamines and other L-tyrosine derivatives at the cloned mouse adrenergic receptors.

The adrenergic system is a neuromodulatory system whose endogenous ligands are considered to be the catecholamines norepinephrine (NE) and epinephrine (E). Evidence suggests that the catecholamine dopamine (DA) may also activate adrenergic signaling. Further, tyramine (TA) and octopamine (OA) are other monoamines that can be produced in catecholaminergic cells when tyrosine hydroxylase activity is low or absent, as in some genetic mouse models of adrenergic function. Here, we systematically examine the ability of these L-tyrosine-derived monoamines to activate all 10 known isoforms of the cloned mouse adrenergic receptors expressed in Chinese hamster ovary cells. In comparison to NE or E, DA is nearly as efficacious in this system but is from 1 to 4 orders of magnitude less potent. In comparison to DA, OA has roughly equivalent potency but is usually only a partial agonist. TA is either very weak or lacks agonism. Of note, all three mouse alpha(1) receptors increase cAMP, in contrast to results reported for human alpha(1d) receptors. In addition, a 12-amino acid hemagglutinin epitope tag added to the N-terminus of alpha(2) receptors selectively enhances the potency of NE approximately 10- to 100-fold, indicating that caution should be applied when interpreting physiological results from experiments using modified receptors.

Animals↗

PubMed2004

[Effects of normal human bone marrow fibroblastoid stromal cell line on the proliferation of multiple myeloma cell line RPMI8226].

To investigate the effects of normal human bone marrow fibroblastoid stromal cell lines HFCL on the proliferation of multiple myeloma cell lines RPMI8226, the co-culture system of RPMI8226 with HFCL was established, the adhesion ratio was determined by MTT colorimetric assay, growth curves were determined by trypan blue exclusion, the mitotic index (MI) of RPMI8226 cell was observed by Wright-Giemsa staining. Flow cytometry and Western blot were used to study the changes of cell cycle and expression of proliferating cell nuclear antigen (PCNA), respectively. The results showed that in co-culture the adhesion ratio of RPMI8226 after 1 hour was 29.4%; the proliferation of RPMI8226 cell line in direct contact with HFCL cell line was inhibited as compared with RPMI8226 in suspension. No obvious changes were observed in RPMI8226 cell separated by transwell inserts. The percentage of G(1) phase cells of RPMI8226 cell line in direct contact with HFCL was higher than that of RPMI8226 in suspension, and the percentage of S phase cells was lower. Moreover, the MI of RPMI8226 cell line in suspension was higher than that of RPMI8226 cell line in direct contact with HFCL cell. The expression of PCNA in RPMI8226 cell line in suspension was higher than that of RPMI8226 cell in direct contact with HFCL cell. It is concluded that the normal human bone marrow fibroblastoid stromal cell HFCL inhibits the proliferation and progression of cell cycle of multiple myeloma cell line, RPMI8226.

Bone Marrow Cells↗

PubMed2003

Optical properties of nanocrystalline Y2O3:Eu depending on its odd structure.

The structure of nanocrystalline Y2O3:Eu prepared by a combustion reaction was analyzed by XRD and high-resolution electron microscopy. Compared with a large-scale particles, 5-nm Y2O3:Eu particles presented as distorted crystallite and rough surfaces. Luminescent and absorption properties of nano-Y2O3:Eu showed remarkably particle size effects. At Y2O3:Eu particle sizes smaller than 10 nm some new results were observed: (a) a red shift of the charge-transfer-state absorption; (b) new emission bands of Eu3+ in the 5D0 --> 7F2 region; (c) luminescent decay of energy level 5D0 of Eu3+ turning to a two-step exponential; and (d) a pronounced increase in quenching concentration and much lower phonon density compared with those of the bulk material. All these phenomena can be attributed to the effect of the softened lattice and surface state of the nanomaterial. The latter was confirmed by stronger excitation by the host absorption after the surface modification.

Journal Article↗

PubMed2003

[Microsequencing, analysis of molecular weight and amino acid composition for pyrimidine 5'-nucleotidase I of human erythrocytes].

To further explore the mechanism of congenital pyrimidine 5'-nuleotidase I (P5'N-I) deficiency, on the basis of purification of the protein, the molecular weight and amino acid composition were analysed by mass-spectrograph and amino-acid analyzer, microsequencing and bioinformation analysis of P5'N-I were performed after it was hydrolysed by trypsin. The results showed that three fractions were found in the purified P5'N-I and their molecular weights were 26,952.9, 55,476 and 110,938, respectively. The sequence from one of the peptide fragments was I-E-G-P-T-I-R-Q-I-E. The homologous sequence was not found after comparision with the ten-amino-acid sequence in GenBank by blast procedure. Amino acid analysis indicated that P5'N-I was composed of 18 amino acids at least, and 243 amino acid residues. In conclusion, the enzyme might be an allosteric enzyme, there might be homologous dimer or tetramer in physiological status of normal human erythrocyte, the microsequence could be designed as the probe for fishing the genes of interest. The composition of amino acid might be an important information in determination of its protein primary structure.

5'-Nucleotidase↗

PubMed2003

[Effects of human fibroblastoid stromal cell line on proliferation of HL-60 cells and expression of VEGF].

To investigate the effects of normal human bone m arrow fibroblastoid stromal cell line (HFCL) on the proliferation of acute myeloid leukemia cell line HL-60 and expression of vascular endothelial growth factor (VEGF), establishing coculture system of leukemia cell line HL-60 and HFCL, growth data was obtained by cell counting. Mitotic index (MI) was observed under Wright-Giemsa staining. Flow cytometry and Western blot were used as assays for cell cycle and expression of proliferating cell nuclear antigen (PCNA) separately. VE GF levels were evaluated by using commercial ELISA kits. The results showed that compared with HL-60 cells without HFCL cells, the proliferation of HL-60 cells in direct contact with HFCL cells and with HFCL cells separated by transwell was inhibited. The MI of HL-60 cells without HFCL cells was highest followed by HL-60 cells separated by transwell and HL-60 cells in direct contact with HFCL cells. The expression of PCNA in HL-60 cells with HFCL cells were lower than HL-60 cells without HFCL cells. Meanwhile, the percentage of HL-60 cells in G1 phase cocultured with HFCL cells was higher than that without HFCL cells while the percentage of Sphase cells was lower. The levels of VEGF in HL-60 cells with HFCL cells were lower than that in HL-60 cells alone. In conclusion, the normal bone marrow fibroblastoid stromal cells inhibited the proliferation of HL-60 cells as well as the expression of VEGF.

Cell Cycle↗

PubMed2002

[Novel quantitative method for evaluating oxygen/glucose deprivation-induced injury of hippocampal slices]

OBJECTIVE: To establish a simple, sensitive in vitro method to evaluate oxygen/glucose deprivation (OGD)-induced injury of brain hippocampal slices in rats. METHODS: Rat hippocampal slices were incubated in 2% 2, 3, 5-triphenyltetrazolium chloride (TTC) solution after oxygen/glucose deprivation. They were then soaked in a measured volume of ethanol and dimethylsulfoxide (50:50) to extract the TTC formazan Product which was then measured by spectrophotometry. OGD induced LDH release was simultaneously measured. RESULTS: Progressive prolongation of OGD induced hippocampal injury resulted in decreased formazan coloration as determined by spectrophotometry. There was a parallel increase in LDH release, thus a negative correlation in these two products was noted. (r=-0.933,P <0.01). The injury was attenuated in the brain slices pre-treated with nimodipine, dexamethasone, and ketamine, but not ONO-1078. CONCLUSION: Solvent extraction and spectrophotometric quantification of formazan represents an objective measurement of OGD-induced injury of rat hippocampal slices.

Journal Article↗

PubMed2002

VCAM-1 expression, eosinophil infiltration, and pharmacological modulation in rat allergic airway inflammation.

AIM: To determine vascular cell adhesion molecule-1 (VCAM-1) expression and eosinophil infiltration in the lungs of the rats with allergic airway inflammation, and their possible modulation by dexamethasone and neurokinin-1 receptor antagonist SR140333. METHODS: Sensitized rats were challenged with inhalation of 1 % ovalbumin aerosol. Protein expression of VCAM-1 in the lungs and eosinophil infiltration around bronchi in different groups were determined 24 h after challenge. SR140333 (0.01 and 0.10 mg/kg) and dexamethasone (0.50 mg/kg) were injected ip, twice a day, for 3 d before challenge. RESULTS: The expression of VCAM-1 was increased in the sensitized rat lungs as compared with the non-sensitized rats (P<0.05). The increment was inhibited by pretreatment with dexamethasone (P<0.05), but not with SR140333 (P>0.05). On the other hand, antigen challenge in sensitized rats evoked eosinophil infiltration (P<0.05) but no further increase in VCAM-1 expression (P>0.05). Furthermore, SR140333 inhibited eosinophil infiltration (P<0.05) but had no effect on VCAM-1 expression (P>0.05), whereas dexamethasone inhibited both responses (P<0.05). CONCLUSION: The expression of VCAM-1 increases during antigen sensitization in rat lungs, and dexamethasone and SR140333 may inhibit allergic airway inflammation in different mechanisms.

Animals↗

PubMed2002

Neuroprotective effect of ONO-1078, a leukotriene receptor antagonist, on focal cerebral ischemia in rats.

AIM: To determine whether ONO-1078 (pranlukast), a potent leukotriene receptor antagonist, has neuroprotective effect on focal cerebral ischemia in the rat. METHODS: Focal cerebral ischemia was induced by 30 min of middle cerebral artery (MCA) occlusion and followed by 24 h reperfusion. ONO-1078 (0.003-1.0 mg/kg) or vehicle (saline 1 mL/kg) was ip injected 30 min before MCA occlusion and 2 h after reperfusion. The neurological score, infarct volume, neuron density (in cortex, hippocampus, and striatum), brain edema, and albumin exudation around the vessels were determined 24 h after reperfusion. RESULTS: ONO-1078 slightly improved the neurological deficiency, and dramatically decreased infarct volume and neuron loss which showed a bell shaped dose response effect with highest effect at doses of 0.01-0.3 mg/kg. Enlargement of the ischemic hemisphere and albumin exudation were inhibited at doses of 0.01-1.0 mg/kg. CONCLUSION: ONO-1078 has the protective effect on focal cerebral ischemia in rats, which is partially attributed to the inhibition of brain edema. This may represent a novel approach to the treatment of acute cerebral ischemia with cysteinyl leukotriene receptor antagonists.

Animals↗

PubMed2002

[Role of interleukin-18 in pathogenesis of acute graft-versus-host disease].

To investigate the relationship between interleukin-18 (IL-18) and human acute graft-versus-host disease (aGVHD), 26 patients undergoing allogeneic peripheral blood stem cell transplantation (allo-PBSCT) were included in this study. IL-18 secreted by peripheral blood mononuclear cells (MNCs) was measured by enzyme-linked immunosorbent assay (ELISA) before transplantation and during aGVHD. The results showed that grade I GVHD and grades III-IV GVHD developed in 10 and 5 cases, respectively. The levels in the supernatants of MNCs from patients with aGVHD were significantly higher than those in the cases without aGVHD. The levels of IL-18 were correlated with the severity of aGVHD. It is concluded that IL-18 plays an important role in the development of aGVHD.

Acute Disease↗