Biomedical subjects

Fangping Chen

Publications and source records attributed to Fangping Chen.

5 recordsLinked to original sources

PubMed2006

Short courses of low dose dexamethasone delay bleomycin-induced lung fibrosis in rats.

After comparing mortality and clinical signs in rats receiving different dexamethasone treatments, we investigated whether 0.5 mg/kg/d dexamethasone could delay pulmonary fibrosis induced by bleomycin and its time course (1, 3, 7, 14, 21 and 28 days). Tissue injury was assessed by apoptosis, lactate dehydrogenase (LDH) release, malondialdehyde content, and protein content; and inflammation was measured in terms of myeloperoxidase (MPO) activity, inflammatory cell count, and the mRNA expression of pro/inflammatory cytokines. Fibrogenic activity was analyzed by measuring the mRNA expression of fibrotic cytokines in tissue, and the promotion of fibroproliferation and synthesis of collagen type I by bronchoalveolar lavage fluids in vitro; and fibrosis was assessed by measuring the hydroxyproline content and collagen-I mRNA expression, and by histology. Bleomycin treatment induced tissue injury, inflammation and fibrogenic activity in lung, and led to fibrosis. Treatment with dexamethasone diminished the extent of fibrosis by strongly reducing inflammation, lung damage, and fibrogenic activity. These results demonstrate that the progression of bleomycin-induced pulmonary fibrosis in rats can be delayed by dexamethasone treatment, which appeared to alleviate not only inflammation but also lung damage and fibrogenic activity, indicating a possible new role for dexamethasone in the treatment of fibrosis.

Animals↗

PubMed2006

Selective inhibition of matrix metalloproteinase isozymes and in vivo protection against emphysema by substituted gamma-keto carboxylic acids.

The synthesis and matrix metalloproteinase (MMP) inhibitory activity of a series of gamma-keto carboxylic acids are described. Among nine MMP isozymes tested, compound 1j displays selective inhibition of MMP-2, -9, and -12 with IC(50) values between 0.20 and 1.51 microuM, and in male golden Syrian hamsters, it shows protection against PPE-induced emphysema.

Animals↗

PubMed2006

Development of quartz-crystal-microbalance-based immunosensor array for clinical immunophenotyping of acute leukemias.

An integrated piezoelectric immunosensor array has been developed to immunophenotype acute leukemias in clinic. Each quartz crystal microbalance (QCM) was fabricated with plasma-polymerized film of n-butylamine, nanogold particles, and protein A (PA) to be used to immobilize antibodies in orientation. Leukemic lineage-associated monoclonal antibodies were separately immobilized onto the nanogold-PA-modified surface of the crystals, which were constructed by a 2 x 2 type of probes forming a QCM-based immunosensor array. The main detection conditions were investigated, including the immobilization amount of antibodies, pH, immunoreaction time, sample dilution ratio, etc. The immunophenotyping feasibility of the new technique was investigated through simultaneously analyzing Jurkat cells by the immunosensor array method, immunohistochemistry, and flow cytometry. It was found that the developed technique could readily identify leukemia samples in 5 min and might monitor dynamically the immunoreaction processes. Moreover, comparison studies were carried out for CD antigens expressed on the nucleated cells isolated from 96 acute leukemic patients and 24 normal subjects using the QCM-based immunosensor method and the fluoroimmunoassay. Results obtained by immunophenotyping patients' samples with the immunosensor-based method achieved the rate of 88.93% in 768 groups of numerical data, where no significant statistical difference was observed between the two methods when checked by chi2 analysis (chi2 = 3.4, p > 0.05). This new immunosensor array showed the merits of high sensitivity, high specificity, good reproducibility, easy operation, and low cost. The results of specimen evaluation indicated that it might be clinically suitable for quantifying human differentiated leukocytes and immunophenotyping of acute leukemias.

Acute Disease↗

PubMed2005

Angiotensin II induces the expression of tissue factor and its mechanism in human monocytes.

The renin-angiotensin system (RAS) is linked with the vascular motion and the secretion of aldosterone. The purpose of the present study was to elucidate whether angiotensin II (Ang II) induces monocytes (Mo) to express tissue factor (TF) and if Ang II subtype 1 receptor (AT1R) antagonists inhibit the effect of Ang II. The roles of different intracellular signal transduction pathways and IkappaB/NF-kappaB in Ang II-induced TF expression of Mo were also studied to explore the mechanisms involved. Mo were isolated from heparinized human blood by a two-step gradient centrifugation, cultured in RPMI-1640 and exposed to Ang II and other test reagents. Mo TF activity and TF antigen were determined with a one-stage clotting method and ELISA, respectively, after the culture. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the TF mRNA levels in Mo. The level of IkappaBalpha in Mo was detected by Western blot analysis. Electrophoresis mobility shift assay (EMSA) was performed to evaluate the binding activity of NF-kappaB in Mo. The experiment results are as follows: (1) Ang II (10(-10)-10(-7) M) induced Mo to express TF activity but had no marked effect on other mononuclear cells. Ang II 10(-10)-10(-7) M) also caused increased TF mRNA expression and TF antigen from Mo in a dose-dependent manner. The TF antigen of Mo was elevated at 4 h after Mo was exposed to Ang II (10(-7) M) in culture, reached the peak at 6 h, and then declined from 12 h. The changes of TF activity were positively correlated with those of TF antigen. TF mRNA expression was elevated at 1 h, peaked at 3 h, and declined after 8 h. (2) Losartan (10(-6)-10(-5) M) significantly inhibited the stimulative effects of Ang II on TF activity, TF antigen and TF mRNA in Mo in a dose-dependent manner. (3) The protein kinase C (PKC) inhibitor, staurosporine, and the protein tyrosine kinase (PTK) inhibitor, genistein, both lowered TF levels in Mo, but the inhibitory effect of staurosporine was stronger than that of genistein. The effect of mitogen-activated protein kinase (MAPK) inhibitor, U0126, on monocytic TF expression was not significant. (4) Western blot analysis revealed that after Ang II (10(-7) M)exposure, levels of IkappaBalpha began to decrease at 15 min, reached a nadir at 60 min (P<.01), and recovered at 180 min. (5) EMSA showed that NF-kappaB binding activity started to increase at 15 min, reached a peak at 60 min, and returned to baseline at 180 min. The present data suggest that Ang II can directly induce TF expression in human Mo and this effect is mediated by AT1R. PKC may play the most important role in Ang II-induced TF expression among the three signal pathways detected. In addition, activation of NF-kappaB is also involved in the TF expression of Mo induced by Ang II.

Angiotensin II↗

PubMed2002

Observation on tissue factor pathway and some other coagulation parameters during the onset of acute cerebrocardiac thrombotic diseases.

It is widely recognized that thrombosis is the major event in the evolution of acute myocardial infarction (AMI) and acute ischemic stroke (AIS). But the contribution of coagulation factors to the development of ischemic arterial diseases is still not clearly established. The goal of this study was to establish the possible relationship between coagulation factors as well as anticoagulant and the onset of AMI and AIS. The study population consisted of 69 patients with AMI and 71 with AIS as well as 50 age-matched healthy volunteers. Compared with the control group, plasma tissue factor (TF) and tissue factor pathway inhibitor (TFPI) activities and both TF and TFPI antigens were significantly higher in the AMI group; plasma TF activity and antigen in AIS group were significantly increased, but the activity and antigen of plasma TFPI were significantly decreased in the AIS group. Plasma FVII coagulation (FVII:C) activity was markedly higher in patients with AIS, but not statistically different to the control in patients with AMI. FVIII coagulation (FVIII:C) activity was remarkably higher in patients with AMI but slightly lower than the control in patients with AIS. In the AMI and AIS groups, prothrombin activity and clottable fibrinogen were significantly higher and plasma antithrombin III activity was remarkably lower than the control. The results suggested that during the onset of AMI and AIS, the initiation of TF pathway would be associated with the thrombotic events and that the blood be in hypercoagulable state. But the changes of FVII:C, TFPI and FVIII:C in AMI are different from those in AIS.

Acute Disease↗