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Shuang Qiu

Publications and source records attributed to Shuang Qiu.

7 recordsLinked to original sources
PubMed2006

Atractyloside and 5-hydroxydecanoate block the protective effect of puerarin in isolated rat heart.

The aim of the present study was to determine whether the clinically effective cardioprotection conferred by puerarin (Pue) against ischemia and reperfusion is mediated by mitochondrial transmembrane pores and/or channels. Hearts isolated from male Sprague-Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The production of formazan, which provides an index of myocardial viability, was measured by absorbance at 550 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was determined. In this model, Pue (0.0024-2.4 mmol/l) had a dose-dependent, negatively inotropic effect. Pretreatment with Pue at 0.24 mmol/l for 5 min before ischemia increased myocardial formazan content, reduced LDH release, improved recovery of left ventricular end-diastolic pressure and rate-pressure product (left ventricular developed pressure multiplied by heart rate) during reperfusion. Administration of atractyloside (20 micromol/l), an opener of the mitochondrial permeability transition pore, for the first 20 min of reperfusion, and 5-hydroxydecanoate (100 micromol/l), the mitochondrial-specific ATP-sensitive potassium channel blocker, for 20 min before ischemia, attenuated the protective effects of Pue. In mitochondria isolated from hearts pretreated with 0.24 mmol/l Pue for 5 min, a significant inhibition of Ca(2+)-induced swelling was observed, and this inhibition was attenuated by 5-hydroxydecanoate. In isolated ventricular myocytes, pretreatment with Pue prevented ischemia-induced cell death and depolarization of the mitochondrial membrane, and atractyloside and 5-hydroxydecanoate attenuated the effects of Pue. These findings indicate that puerarin protects the myocardium against ischemia and reperfusion injury via inhibiting mitochondrial permeability transition pore opening and activating the mitochondrial ATP-sensitive potassium channel.

Animals↗
PubMed2006

[Tyroservatide inhibits the growth of human hepatocarcinoma in nude mice].

OBJECTIVE: To investigate the inhibitory effects of tyroservatide and its amino acid mixture on growth of hepatocarcinoma. METHODS: Hepatocarcinoma in nude mice was induced by implantation of cells of human hepatocarcinoma cell line BEL-7402. The inhibition of hepatocarcinoma growth was determined by calculating the tumor volume and measuring the tumor weight. The effects of tyroservatide on tumor cells in nude mice were assessed by immunohistochemical staining of proliferating cell nuclear antigen (PCNA), electron microscopic observation of ultrastructure, and apoptosis of tumor cells using terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL). RESULTS: Tyroservatide significantly inhibited the growth of human hepatocarcinoma in nude mice, with an inhibiting rate more than 60%. But the mixture of amino acid did not show a significant inhibitory effect on the tumor growth. Tyroservatide also induced apoptosis of tumor cells and decreased the expression of PCNA in tumor cells. CONCLUSION: Tyroservatide may significantly inhibit the growth of human hepatocarcinoma in nude mice by inducing apoptosis and inhibiting proliferation of tumor cells.

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PubMed2005

Tripeptide tyroserleutide enhances the antitumor effects of macrophages and stimulates macrophage secretion of IL-1beta, TNF-alpha, and NO in vitro.

Tyroserleutide (YSL) is a type of active, low molecular weight polypeptide, comprised of three amino acids, which has antitumor effects. YSL has various advantages over the other bioactive peptides such as its low molecular weight, simple construction, nonimmunogenicity, specificity, few side effects, and ease of synthesis. However, the biological activities contributing to it's antitumor effects are not yet known. We studied the effects of YSL on the in vitro cytotoxic activity of BALB/c mice peritoneal macrophages (PEMphi) against the target tumor cell lines BEL-7402 and B16-F10. We also measured the concentrations of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and nitric oxide (NO) produced by YSL-activated Mphi, and we determined the concentrations of IL-1beta and NO secreted by YSL-activated murine macrophage RAW264.7 cells. YSL activated Mphi in vitro, inhibited BEL-7402 proliferation, enhanced PEMphi antitumor effects, and stimulated IL-1beta, TNF-alpha, and NO production by RAW264.7 cells. These data suggest that YSL activates the monocyte-macrophage system, which enhances Mphi antitumor effects against BEL-7402 and B16-F10 cells and stimulates the secretion by Mphi of cytotoxic effectors such as IL-1beta, TNF-alpha, and NO.

Animals↗
PubMed2005

Preliminary investigation of the inhibitory effects of the tyroservaltide (YSV) tripeptide on human hepatocarcinoma BEL-7402.

This study aimed to investigate the inhibitory effect of tyroservaltide (YSV) on the human hepatocarcinoma BEL-7402 transplanted into nude mice and to explore its possible anti-tumor mechanism. Nude mice bearing xenografts of the human BEL-7402 hepatoma were given daily i.p. injections of YSV or saline (as a control) after the tumor were transplanted. Calculating tumor volume and measuring tumor weight determined the extent of inhibition of xenografts. The ultrastructure of tumor cells was observed by electron microscopy. Proliferating cell nuclear antigen (PCNA) expression in tissues of the YSV-treated group was observed by immunohistochemistry. Apoptosis of tumor tissue cells was assayed by the terminal transferase uridyl nick end labeling (TUNEL) method. At doses of 80 microg/kg/d and 160 microg/kg/d, YSV could significantly inhibit growth of tumors transplanted into nude mice, with inhibition rates of 60% and 64%, respectively, compared with that of the controls (P < 0.05). Moreover, YSV changed the ultrastructure of tumor cells, resulting in necrosis and apoptosis of the tumor cells. Compared with the saline group, the expression of PCNA in tumor tissue decreased and the count of apoptotic cell increased. Therefore, YSV can significantly inhibit the growth of human hepatocarcinoma BEL-7402 in nude mice, decrease the expression of PCNA in tumor tissue, and induce tumor cell apoptosis.

Animals↗
PubMed2005

Subunit assembly of N-methyl-d-aspartate receptors analyzed by fluorescence resonance energy transfer.

N-methyl-d-aspartate (NMDA) receptors play major roles in synaptic transmission and plasticity, as well as excitotoxicity. NMDA receptors are thought to be tetrameric complexes mainly composed of NMDA receptor (NR)1 and NR2 subunits. The NR1 subunits are required for the formation of functional NMDA receptor channels, whereas the NR2 subunits modify channel properties. Biochemical and functional studies indicate that subunits making up NMDA receptors are organized into a dimer of dimers, and the N termini of the subunits are major determinants for receptor assembling. Here we used a biophysical approach, fluorescence resonance energy transfer, to analyze the assembly of intact, functional NMDA receptors in living cells. The results showed that NR1, NR2A, and NR2B subunits could form homodimers when they were expressed alone in HEK293 cells. Subunit homodimers were also found existing in heteromeric NMDA receptors formed between NR1 and NR2 subunits. These findings are consistent with functional NMDA receptors being arranged as a dimer of dimers. In addition, our data indicated that the conformation of NR1 subunit homodimers was affected by the partner NR2 subunits during the formation of heteromeric receptor complexes, which might underlie the mechanism by which NR2 subunits modify NMDA receptor function.

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PubMed2003

[Surface expression and co-localization of NMDA receptor and AMPA receptor on dendritic tree of hippocampal neurons in culture].

OBJECTIVE: To investigate the developmental profiles on surface expression and co-localization of NMDA receptor clusters and AMPA receptor clusters on dendrite in cultured hippocampal neurons of rats. METHODS: Green fluorescent protein tagged GluR2 subunit (GFP-GluR2) and FLAG tagged NR2B subunit (FLAG-NR2B) were transfected into cultured hippocampal neurons at 5 days in vitro (DIV5). FLAG-NR2B containing NMDA receptor clusters and GFP-GluR2 containing AMPA receptor clusters expressed on membrane surface were then labeled in living neurons using anti FLAG mAb/Cy3-conjugated anti-mouse antibody and anti-GFP pAb/Alex488-conjugated anti-rabbit antibody. RESULT: The numbers of receptor cluster per 100 microm dendrite in the neurons at DIV7 and DIV19 were 39.7+/-5.0 and 64.7+/-6.1 (P<0.01) for NR2B-NMDAR, 59.1+/-3.3 and 99.7+/-6.4 (P<0.01) for GluR2-AMPAR, and 29.9+/-4.5 and 37.5+/-2.5(P<0.05) for the co-localized, respectively. At DIV7 and DIV19, 75.4% and 57.9% NR2B-NMDAR clusters were co-localized with GluR2-AMPAR; and 50.6% and 37.6% GluR2-AMPAR clusters were co-localized with NR2B-NMDAR, respectively. CONCLUSION: The density of NR2B-NMDAR containing and GluR2-AMPAR containing receptor clusters increases during development of hippocampal neurons in culture. Although the co-localized clusters are increased as well in an unit length of dendrite, the extent to which the two receptor clusters are co-localized decreases. These data imply a possible change in the partnership of AMPA receptor subtype and NMDA receptor subtype at newly formed synapses during development.

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