Publications by authors named "Xian-Da Ren"

Aim: To investigate whether total Panax notoginseng saponins (PNS) could protect endothelium of rabbit iliac artery against balloon endothelial denudation (BED) injury.

Methods: The morphology changes of the endothelium were observed with scanning electron microscope (SEM) and hematoxylin and eosin stain after BED of rabbit iliac artery at 0, 4, 6, and 8 week respectively. Vascular endothelial growth factor (VEGF) and matrix metalloproteinase-2 (MMP-2) was also determined by immunohistochemistry.

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Aim: To investigate the changes of function of large conductance of calcium-activated potassium channels (BK(Ca) channels) in thoracic aortic smooth muscle cells in early stage of streptozotocin (STZ)-induced diabetic C57BL/6J mice.

Methods: Vascular muscle tension in the isolated thoracic aortic rings of mice was compared, and the role of BK(Ca) channels in relaxation of isolated mice thoracic aortic rings induced by acetylcholine (ACh) was determined. Meanwhile, single vascular smooth muscle cells (VSMCs) were isolated by collagenase, and BK(Ca) currents were recorded by patch-clamp single channel recording technique in symmetric high potassium solution.

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Aim: To investigate the possibility that a novel alpha-helix-defective mutant of stromal cell-derived factor-1alpha (SDF-1alpha) (SDF-1/54R) acts as an antagonist of CXC chemokine receptor 4 (CXCR4).

Methods: According to the genetic sequence of natural SDF-1alpha, a recombinant alpha-helix-defective mutant of SDF-1alpha was designed and some biologic characteristics of this mutant were demonstrated. The migration of Jurkat cells was assessed with chemotactic assay.

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Aim: To investigate the inhibitory effect of serum preparation from rabbits orally administered cobra venom (SRCV) on implanted hepatocellular carcinoma (HCC) cells in mice.

Methods: An HCC cell line, HepA, was injected into mice to prepare implanted tumors. The animals (n=30) were divided randomly into SRCV, 5-fluorouracil (5-FU), and distilled water (control) groups.

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Aim: To investigate whether nimesulide could suppress tumor growth and induce apoptosis in implanted hepatoma mice and to explore the molecular mechanisms.

Methods: Male mice received nimesulide 10 mg/kg, 20 mg/kg, and 40 mg/kg ig daily for 21 d. Electron microscopy (EM), flow cytometry (FCM), DNA ladder, radioimmunoassay (RIA), and Western blot analysis were employed to investigate effect of nimesulide on mice hepatoma and the related molecular mechanisms.

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Aim: To compare the effect of nimesulide or/and 5-fluorouracil (5-FU) on tumor growth inhibition and apoptosis in mice with the implanted hepatoma and to observe their possible interactions.

Methods: The inhibitory effects on tumor growth was evaluated by inhibition rate. Apoptosis was assessed by the ultrastructural, flow cytometry features and the DNA ladder demonstrated by agarose gel electrophoresis.

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Aim: To investigate whether JTE-522 [4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide], a selective COX-2 inhibitor, can induce apoptosis and inhibit cell proliferation in human endometrial cancer cell line RL95-2 cells and to explore the molecular mechanisms.

Methods: [3-(4,5)-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), DNA ladder, enzyme-linked immunosorbent assay (ELISA), flow cytometry, RT-PCR, and Western blot analysis were employed to investigate effect of JTE-522 on human endometrial cancer cell line RL95-2 cells and the related molecular mechanisms.

Results: JTE-522 inhibited the growth of RL95-2 cells and induced the apoptosis.

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Aim: To identify whether JTE-522 can induce apoptosis in AGS cells and ROS also involved in the process, and to investigate the changes in NF-kB, p53, bcl-2 and caspase in the apoptosis process.

Methods: Cell culture, MTT, Electromicroscopy, agarose gel electrophoresis, lucigenin, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanisms.

Results: JTE-522 inhibited the growth of AGS cells and induced the apoptosis.

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Aim: To investigate the role of the mitochondrial pathway in JTE-522-induced apoptosis and to investigate the relationship between cytochrome C release, caspase activity and loss of mitochondrial membrane potential (Deltapsim).

Methods: Cell culture, cell counting, ELISA assay, TUNEL, flow cytometry, Western blot and fluorometric assay were employed to investigate the effect of JTE-522 on cell proliferation and apoptosis in AGS cells and related molecular mechanism.

Results: JTE-522 inhibited the growth of AGS cells and induced the apoptosis.

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Aim: To measure the effect of addition of heparin to adriamycin (ADM) on cell proliferation and apoptosis in CNE2 cells and investigate the possible molecular mechanisms of heparin and ADM interactions.

Methods: Cell viability and cell cycle were determined by MTT assay and flow cytometry. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and agarose gel electrophoresis.

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