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ABSTRACT: Aim:To investigate the effects of salvianolate, a water-soluble active compound from Salvia miltiorrhiza Bunge, on reactive oxygen species (ROS) production in mouse cardiomyocytes in vitro.Methods:Primary ventricular cardiomyocytes were prepared from neonatal mouse. The cell viability was determined using MTT assay. Culture medium for each treatment was collected for measuring the levels of NO, iNOS, total antioxidant capacity (TAOC) and transforming growth factor β1 (TGFβ1). TGFβ1 and Smad2/3 expression in the cells was detected with Western blotting.Results:H2O2 (1.25 mmol/L) did not significantly affect the cell viability, whereas the high concentration of salvianolate (5 g/L) alone dramatically suppressed the cell viability. Treatment of the cells with H2O2 (1.25 mmol/L) markedly increased ROS and iNOS production, and decreased the levels of NO, TAOC and TGFβ1 in the culture medium. Furthermore, the H2O2 treatment significantly increased TGFβ1 and Smad2/3 expression in the cells. Addition of salvianolate (0.05, 0.1, and 0.5 g/L) concentration-dependently reversed the H2O2-induced alterations in the culture medium; addition of salvianolate (0.05 g/L) reversed the H2O2-induced increases of TGFβ1 and Smad2/3 expression in the cells. Blockage of TGFβ1 with its antibody (1 mg/L) abolished the above mentioned effects of salvianolate.Conclusion:Salvianolate inhibits ROS and iNOS production and increases TAOC and NO levels in H2O2-treated cardiomyocytes in vitro via downregulation of Smad2/3 and TGFβ1 expression. High concentration of salvianolate causes cytotoxicity in mouse cardiomyocytes.
Acta Pharmacologica Sinica 03/2013; · 1.95 Impact Factor
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ABSTRACT: To analyze the value of automated acid-base mapping on diagnose and treatment of patients with community acquired pneumonia (CAP) in emergency department.
According to medical history, pulmonary function test, diagnosing guideline of chronic obstructive pulmonary disease (COPD), 111 patients with CAP were divided into two groups: single CAP group (n=56) and COPD complicated with CAP group [acute exacerbation of chronic obstructive pulmonary disease (AECOPD) group, n=55]. After enquiring medical history, arterial blood samples were drawn for blood gas analysis and automated acid-base mapping was analyzed.
Arterial blood gas analysis showed arterial carbondioxide partial pressure (PaCO(2)), HCO(3)(-), base excess of AECOPD group were obviously higher than those in CAP group (PaCO(2): 7.714±2.414 kPa vs. 5.896±1.308 kPa, HCO(3)(-): 30.767±7.185 mmol/L vs. 25.014±3.043 mmol/L, BE: 4.345±5.371 mmol/L vs. -0.354±3.180 mmol/L, all P<0.01). Automated acid-base mapping showed acid-base disturbance of AECOPD group was 89.1% and CAP group was 66.1%. Chi-square analysis were done for patients of normal (10.9%, 33.9%), acute respiratory acidosis (12.7%, 14.3%), chronic respiratory acidosis (49.1%, 10.7%), respiratory alkalosis (7.3%, 14.3%), metabolic acidosis (12.7%, 17.9%), metabolic alkalosis (12.7%, 8.9%) between AECOPD group and CAP group, and statistical significance was found between AECOPD group and single CAP group (χ (2)=24.421, P=0.001). Advanced Chi-square analysis for patients of normal, acute respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis were done and showed no statistical difference (χ (2)=5.280, P=0.260). It is indicated chronic respiratory acidosis occurrences rate in AECOPD patients was higher than single CAP patients.
Our study demonstated that automated acid-base mapping may be helpful for emergency physician to rapidly recognize multi-acid-base disturbance in patients with CAP, and to promptly indentify acute or chronic phase of respiratory disease.
Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 10/2012; 24(10):600-3.
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ABSTRACT: Over-expressed CHMP5 was found to act as oncogene that probably participated in leukemogenesis. In this study, we constructed the CHMP5 single chain variable fragment antibody (CHMP5-scFv) retrovirus and studied the changes of programmed cell death (PCD) of AML leukemic cells after infection by the retrovirus.
The anti-CHMP5 KC14 hybridoma cell line was constructed to generate monoclonal antibody of CHMP5. The protein expression of CHMP5 was studied using immunofluorescence analysis. pMIG-CHMP5 scFv antibody expressible retroviral vector was constructed to prepare CHMP5-scFv retrovirus. AML leukemic U937 cells were infected with the retrovirus, and programmed cell death was studied using confocal microscope, FCM and Western blot.
We obtained a monoclonal antibody of CHMP5, and found the expression of CHMP5 was up-regulated in the leukemic cells. After U937 cells were infected with CHMP5-scFv retrovirus, CHMP5 protein was neutralized. Moreover, the infection resulted in a significant increase in apoptosis and necrosis of U937 cells. In U937 cells infected with CHMP5-scFv retrovirus, apoptosis-inducing factor (AIF)-mediated caspase-independent necrotic PCD was activated, but autophagic programmed cell death was not observed. Neither the intrinsic nor extrinsic apoptotic PCD pathway was activated. The granzyme B/perforin-mediated caspase-dependent apoptotic PCD pathway was not activated.
CHMP5-scFv retrovirus can neutralize the abnormally high levels of the CHMP5 protein in the cytosol of AML leukemic U937 cells, thereby inducing the programmed cell death of the leukemic cells via AIF-mediated caspase-independent necrosis and apoptosis.
Acta Pharmacologica Sinica 05/2012; 33(6):809-16. · 1.95 Impact Factor
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ABSTRACT: The high expression of tissue factor (TF) is related to the coagulation disorder in acute leukemia. TF in blood circulation is mainly expressed in cells, microparticles (MP) and alternatively spliced human tissue factor (asHTF). To elucidate the role of TF in the coagulation disorder of acute myeloid leukemia (AML), RT-PCR was performed on 6 common AML cell lines NB4, HL-60, Kasumi-1, U937, K562 and THP-1. The results showed that only NB4 and U937 cells expressed baseline full-length TF and asHTF which were proved by sequencing. The flow cytometric detection, TF activity and TF antigen tests in NB4 and U937 cells revealed that the asHTF was expressed in trace amount and almost had no activity, while the TF antigen and activity in microparticles were significantly higher than that in asHTF. It is concluded that asHTF may play an unimportant role in the coagulation disorder of AML. Microparticle associated tissue factor (MP-TF) is the predominant source of TF activity released from AML cells.
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 03/2011; 19(2):288-92.
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ABSTRACT: In this study, we evaluated SEA-H61D, a staphylococcal enterotoxin A mutant without emetic activity, as an antitumor agent in vitro and in vivo. It showed that SEA-H61D could significantly inhibit the growth of many cancer cell lines in vitro at very low concentrations by activating human peripheral blood mononuclear cells (PBMCs). CD4+ and CD8+ T lymphocytes could be activated at a dose between 125 and 500 μg/kg. Systemic administration of SEA-H61D in vivo significantly inhibited tumor growth, with the treated group undergoing tumor necrosis and showing a strong infiltration of lymphocytes to the tumor area.
Cancer Investigation 10/2010; 28(8):788-96. · 1.85 Impact Factor
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ABSTRACT: The expression pattern of microRNAs (miRNAs) and their potential target genes were investigated in acute promyelocytic leukemia (APL) cell line NB4 cells during all-trans-retinoid acid (ATRA) treatment by using a miRNA microarrays platform and real-time quantitative PCR (RTQ-PCR). MiR-146a as one of the miRNAs down-regulated by ATRA during APL differentiation was identified. Direct interaction between miR146a and its predictive target gene Smad4 were confirmed by Luciferase assay. Down-regulation of miR-146a and upregulation of Smad4 at protein levels were demonstrated. These data suggested that miR-146a might influence proliferation of APL cells through TGF-beta1/Smad signal transduction pathway during ATRA induction.
International journal of hematology 07/2010; 92(1):129-35. · 1.17 Impact Factor
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ABSTRACT: This study was purposed to prepare and primarily identify the specific monoclonal antibodies (McAbs) against the apoptosis related protein PNAS-2 so as to provide the essential tool for study of PNAS-2 function. The McAbs against PNAS-2 were prepared via the immunization of mice, cell fusion and cloning using synthetic peptide of PNAS-2 as immunogen; the specificity, titer and subtype of McAb were detected by Western blot, ELISA and immunofluorescence. The results showed that the stable hybridoma cell line S-31-7 producing McAbs against PNAS-2 protein was successfully obtained. The immunoglobulin of the McAb was identified to be IGg1lambda. The titer of ascetic fluid fled McAb were 1:8,000. A single specific band with 28 kD was shown in Western blot test, and the antigen recognized was present in cell cytoplasm by immunofluorescence. In conclusion, the obtained McAb against PNAS-2 displays strong specificity and high titer, which may be applied to the advanced research on PNAS-2 protein.
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 10/2009; 17(5):1269-72.
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ABSTRACT: The aim of the study was to present the possible mechanisms of transforming growth factor beta 1(TGF-beta1) signal pathway during cell differentiation by studying the expression levels of six components of TGF-beta1 pathway (TGF-beta1, two TGF-beta1 receptors and three Smad proteins). The morphology change, the CD11 expression levels, and the mRNA and protein expression levels of TGF-beta1, TGF-beta ReceptorI (TbetaRI), TGF-beta ReceptorII (TbetaRII), Smad2, Smad4 and Smad7 were assessed by exposing NB4 cells to all-trans retinoid acid (ATRA) using Wright's stain, flow cytometry, real-time PCR assay and Western blot analysis. The mRNA and protein expression levels of all six components increased during NB4 cells differentiation induced by ATRA. They were most significantly increased after 24-72 h individually when cells were induced by ATRA (the mRNA and protein expression levels of TGF-beta1, TbetaRI, TbetaRII and Smad2 reached their peaks at 48 and 48 h individually after the treatment, Smad4 at 48 and 72 h, and Smad7 at 72 and 72 h). The change in mRNA expression levels was earlier than the change in the same gene controlling protein. These results indicate that the upregulation of TGF-beta1 pathway plays an important role in NB4 cells differentiation induced by ATRA.
International journal of hematology 05/2009; 89(4):438-44. · 1.17 Impact Factor
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ABSTRACT: To explore the expression spectra of apoptosis-related gene pnas-2 in normal tissues and acute leukemia (AL) patient tissues, the expressions of pnas-2 gene in tissues including heart, brain, placenta, lung, liver, skeletal muscle, kidney, pancreas, spleen, lymph node, thymus, leukocyte, bone marrow and fetal liver were detected by Northern blot. The expressions of pnas-2 in samples including 44 de novo, 9 non-CR, 27 CR and 12 relapsed AL patients were measured by real-time RT-PCR and Northern blot, and the expression levels of pnas-2 in normal and tumor tissues from 31 patients with malignancies were also detected. The results showed that pnas-2 was not expressed in the most tissues except in placenta. The results of real-time PCR indicated that pnas-2 expressions in samples of de novo, non-CR and relapsed patients ware significantly higher than that in CR, tumor tissues and normal tissues. In serial monitoring of 7 AL patients, the expression level of pnas-2 was high at first visit examination, but remarkably decreased after remission, and the pnas-2 expression level increased again when relapsed. It is concluded that the pnas-2 is specifically up-regulated in acute leukemia patients, which might be an oncogene and participate in leukemogenesis.
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 05/2008; 16(2):282-5.
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ABSTRACT: The objective of study was to investigate the role of the polymorphisms and protein expression of CYP3A5 gene in the therapy and prognosis of acute leukemia (AL) patients, the polymorphisms of CYP3A5 gene and the expression of protein CYP3A5 were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and immunohistochemistry method respectively. The results showed that there were three CYP3A5 genotypes in the 88 cases, namely CYP3A5*1/*1, CYP3A5*1/*3 and CYP3A5*3/*3 with frequencies of 26%, 50% and 24%, respectively. There were no significant differences in clinic data between the three groups, but the expressions of CYP3A5 of three groups were (36.6+/-19.2)%, (7.8+/-9.2)%, (0.5+/-0.9)%, the OS were (11.6+/-2.1) months, (30.5+/-12.2) months, (52.3+/-8.5) months, and the DFS were (7.5+/-1.8), (27+/-15.8), (52.3+/-8.1) months, respectively (p<0.05). It is concluded that the polymorphism of CYP3A5 gene is not related with the morbidity of AL, but closely associated with the expression of CYP3A5 in AL patients, and the latter are closely associated with the chemotherapeutic effect and prognosis. CYP3A5 genotype may be used as a new predictor to the chemotherapeutic effect and prognosis in AL cases.
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 03/2008; 16(1):26-30.
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ABSTRACT: Superantigens tremendously activate T lymphocytes by recognizing the particular region on TCR Vbeta, by which cytotoxic T cells can be well armed to kill tumor cells. However, the obstacle exists in the fact that immunosuppression is induced adversely. Staphylococcal enterotoxins (SEs) are pyrogenic superantigens who invoke T lymphocytes cytotoxicity at a very low dosage where their endotoxic activity diminishes. Despite that the elaborate mechanisms are largely unknown, tumoricidal capacity of SEA and SEB has been well studied. In this study, we devoted our attention to evaluate Staphylococcal Enterotoxin C (SEC) regarding its tumoricidal activity versus immunosuppression. We proved with flow cytometry that SEC treatment on C57 mice resulted in a boost of the differentiation of T lymphocytes into CD4(+), CD8(+) subpopulations. In vitro, SEC causes increased IFNgamma release from human PBMC. Furthermore, in coculture SEC-treated human PBMC led to more death of cancer cell lines from a variety of origins. Systemic SEC treatment in mouse and rabbit models significantly decreases tumor growth. In tumor-bearing rabbits, tumor necrosis and strong infiltration of lymphocytes into tumor tissue were observed; the rabbits also benefit with less metastasic cancer cells in the lung. In the meantime, the induced cell immune responses, both T cell differentiation and PBMC IFNgamma release, declined as SEC concentration rose. Tumor growth data obtained from animal models are in accordance with the changes in immunity, in which tumor growth ceased to respond to high dosage SEC as it did to lower dosage. These observations on SEC investigation, particularly in aspect of dosage-related immunosuppression, are of significance to SEC therapeutic potential to cancer. Molecular mechanism underlying these findings warrants further intensive investigation.
Cancer biology & therapy 11/2007; 6(10):1584-91. · 2.64 Impact Factor
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ABSTRACT: The study was purposed to explore the correlation between apoptosis-related gene pnas-2 and leukemia. The RT-PCR was performed to detect the expression levels of pnas-2 gene in NB4, K562, U937 cells before and after treatment with AS(4)S(4), and to analysis the expression change of pnas-2 gene in bone marrow cells from patients with acute leukemia before and after chemotherapy. The results showed that the expression of pnas-2 gene in arsenic sulfide treated NB4 cells was down regulated in time-dependent manner, but the same outcome in K562 and U937 cells after being treated with AS(4)S(4) was not found. The positive expression rate of pnas-2 in cells from untreated patients with acute leukemia was 100%, and was significantly higher than that in normal control group. After chemotherapy, the expression was negative in complete remission patients, whereas in no-remission patients there were no significant differences of expression of pnas-2 before and after treatment. It is concluded that the pnas-2 gene may be closely related with apotosis of arsenic sulfide treated APL cells, and may consider as a molecular biological remission marker in acute leukemia.
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 09/2007; 15(4):738-42.
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ABSTRACT: To explore whether daunorubicin (DNR) combined with cytosine arabinoside (Ara-C) and DNR alone have similar effect on acute promyelocytic leukemia (APL) cell line NB4 and acute myeloblastic leukemia cell line HL-60 in vitro.
Cell morphology, cells viability, and cell apoptosis (Annexin-V by flow cytometry assay) were analysed.
After incubation with DNR plus Ara-C for 24 hours,NB4 cell viability [(36.75 +/- 3.82)%] (n = 6) and cell apoptosis rate [(21.24 +/- 5.82)%] (n = 3) did not change significantly compared to that treated with DNR alone for 24 hours [(35.73 + 6.28 )%, (22.55 +/- 3.26)%, respectively] (P > 0.05). However, HL-60 cell viability [(67.17 +/- 2.07)%] and cell apoptosis rate [(48.05 +/- 0.92)%] changed significantly in DNR plus Ara-C group compared with DNR alone [(63.31 +/- 1.80)% ,(41.51 +/- 0.89)%, respectively] (P < 0.01 and < 0.05, respectively).
DNR plus Ara-C and DNR alone have similar effect on NB4 cells, but have different effect on HL-60 cells.
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 04/2007; 28(4):247-9.
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ABSTRACT: To investigate the effects of quercetin on cell morphology and VEGF expression of acute myeloblastic leukemia cells NB4 in vitro.
The cytomorphology of NB4 cells was assessed by Wright-stain, apoptosis rate by apoptotic marker Annexin V, and VEGF secretion level by ELISA.
Typical apoptosis was found in NB4 cells after treatment with quercetin. Apoptotic marker Annexin V analysis showed that the apoptotic rate of NB4 cells was increased after treatment with quercetin. The secretion of VEGF of NB4 cells was significantly decreased after treatment with quercetin.
Quercetin can induce apoptosis and inhibit secretion of VEGF in NB4 leukemia cells.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 02/2006; 28(1):25-7.
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ABSTRACT: As(4)S(4) is an effective drug for the treatment of acute promyelocytic leukemia but its mechanism of action remains largely unknown. In a previous study, we identified PNAS-2, a human apoptosis-related protein gene, using gene expression profiling. In this study, we tried to clarify the role of PNAS-2 in apoptosis and leukemogenesis.
NB4 and U937 leukemia cell lines and serial clinical samples were studied. RNA interference (RNAi) and RNA overexpression were used to address the potential role of PNAS-2 in apoptosis. PNAS-2 expression was examined using Northern blot in multiple tissues, and real-time PCR was applied to analyze PNAS-2 expression in various patient samples.
Functional analyses of PNAS-2 by RNAi and RNA overexpression indicate PNAS-2 is an anti-apoptosis gene. PNAS-2 expression is significantly increased in de novo or relapsed acute leukemia, but in patients in complete remission PNAS-2 levels decrease to levels comparable to those found in normal controls. In carcinomas, PNAS-2 expression was not upregulated, indicating that PNAS-2 overexpression was specific for leukemia.
Based on the preliminary data, we suggest that the PNAS-2 gene functions as an anti-apoptotic gene and probably participates in leukemogenesis.
Oncology 02/2006; 71(5-6):423-9. · 2.27 Impact Factor
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ABSTRACT: Inflammation plays a critic role in atherosclerosis and C-reactive protein (CRP) may directly facilitate the development of a proinflammatory and proatheroscleroitc phenotype. The nuclear factor-kappaB (NF-kappaB) signal transduction is known to play a key role in the expression of these proatherogenic entities including tumor necrosis factor-alpha (TNF-alpha). Much data suggest that statin possess a potential anti-inflammatory effect. However, the effects of statin on the expression of TNF-alpha and activation of NF-kappaB in endothelial cells stimulated by CRP are less studied. We determined the effects of CRP in inducing inflammatory response and the effect of fluvastatin on CRP-dependent inflammatory activation in human cultured endothelial cells.
Human vascular endothelial cells were cultured and stimulated by concentrations of CRP (5-100 microg/ml) for 0, 2, 4, 8, 16, 24, and 48 h. Also 10 micromol/l of fluvastatin was pre-incubated for 2 h with cells in the presence of CRP. The activity of transcription factor NF-kappaB was evaluated by electrophoretic mobility shift assay (EMSA). Measurements of TNF-alpha were performed from supernatants of cultured medium in duplicate, using commercial assay kits.
CRP increased the release of TNF-alpha rapidly as a dose-and time-dependent manner. Induction of TNF-alpha was detected at 5 microg/ml and reached a maximum at 100 microg/ml of CRP. The CRP also significantly induces the activation of NF-kappaB in endothelial cells, and those effects were apparently inhibited by 10 micromol/l of fluvastatin, but not complete.
CRP stimulation result in induction of TNF-alpha and activation of NF-kappaB, and this effect could be significantly inhibited by fluvastatin, suggesting that CRP may play a direct role in atherogenesis by activating endothelial cells, and statins inhibit this response, which may provide an insight into the mechanisms of anti-inflammatory or anti-atherosclerotic actions of statins.
Clinica Chimica Acta 04/2005; 353(1-2):53-60. · 2.54 Impact Factor
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ABSTRACT: Previous studies showed that monocytes from patients with unstable coronary disease exhibit a greatly enhanced production of interleukin-6 (IL-6) in response to lipopolysaccharide and artery injury. Moreover, accumulating evidence suggest that C-reactive protein (CRP) may have direct proinflammatory effects on the cells of vascular wall. Whether this enhanced inflammatory response also exists, however, in cultured monocytes from patients with unstable angina, in response to CRP, has not been investigated.
Monocytes were isolated from blood of 15 healthy volunteers (normal control), 15 patients with stable angina, and 15 patients with unstable angina by Ficoll density gradient and were stimulated by 20 microg/ml of CRP for 24 h. Measurements of IL-6 and tumor necrosis factor-a (tnf-alpha) were performed from supernatants of cultured medium in duplicate, using a commercial assay kit.
the data showed that IL-6 and tnf-alpha concentrations of spontaneous secretion (baseline) were higher in patients with unstable angina than in patients with stable angina and normal control (IL-6: 179+/-19 vs. 87+/-6 and 89+/-8 pg/ml, p<0.05, respectively; tnf-alpha: 69+/-13 vs. 30+/-4 and 27+/-3 pg/ml, p<0.05, respectively). CRP induced the enhanced release of IL-6 and tnf-alpha by 17-fold and 23-fold increase, respectively, in patients with unstable angina, while it did about 11-fold and 19-fold increase in patients with stable angina and normal group (IL-6: 3129+/-333 vs. 991+/-134 and 987+/-102 pg/ml, p<0.01, respectively; tnf-alpha: 1554+/-784 vs. 560+/-135 and 558+/-152 pg/ml, p<0.01, respectively).
Increased baseline concentrations of IL-6 and tnf-alpha can be a marker of the hyperresponsiveness of the inflammatory system in patients with unstable coronary disease. CRP could enhance even further this response, suggesting that a persisted and enhanced inflammatory responsiveness to CRP may be involved in the pathogenesis of unstable coronary disease.
Clinica Chimica Acta 03/2005; 352(1-2):127-33. · 2.54 Impact Factor
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ABSTRACT: Hepatocellular carcinoma (HCC), one of the most common and malignant tumors worldwide, is unresponsive to any of the available therapies. Using intact HCC cells as therapeutic targets, we isolated a novel peptide, denoted HCC79 (KSLSRHDHIHHH), from a phage display peptide library. HCC79 can bind to hepatoma cell membranes with high affinity and specificity. Remarkably, competitive binding assays demonstrated that HCC79 competed with HAb25, a specific antibody for HCC, in binding to hepatoma cells. The corresponding synthetic peptide did not inhibit tumor proliferation directly, but repressed tumor invasion significantly in a cell migration assay. Moreover, we explored the potential of the selected peptide to deliver a superantigen (SAg) to cancer cells, to attain a significant cell-targeting effect. When the peptide is fused to the TSST-1 SAg, the resulting fusion protein could bind to hepatoma cells with high affinity in vitro and improved the tumor inhibition effect by activating T lymphocyte cells in vitro and in vivo, compared with TSST-1 alone. Taken together, our results indicate that this peptide and its future derivatives may have the potential to be developed into highly specific therapeutic agents against cancer.
Molecular Medicine 12(4-6):81-7. · 3.76 Impact Factor
