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Biomedical subjects

Ji-fang Sheng

Publications and source records attributed to Ji-fang Sheng.

4 recordsLinked to original sources
PubMed2005

Intestinal microflora in rats with ischemia/reperfusion liver injury.

OBJECTIVES: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. METHODS: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin, intestinal bacterial count, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. RESULTS: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in I/R group compared to those in the sham group. Intestinal Bifidobacterium and Lactobacillus decreased and intestinal Enterobacteria and Enterococci, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group. CONCLUSION: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, which contributes to endotoxemia and bacterial translocation to kidney.

Animals↗
PubMed2005

Phenotypic and functional characteristics of dendritic cells derived from human peripheral blood monocytes.

OBJECTIVE: This study is aimed at developing a simple and easy way to generate dendritic cells (DCs) from human peripheral blood monocytes (PBMCs) in vitro. METHODS: PBMCs were isolated directly from white blood cell rather than whole blood and purified by patching methods (collecting the attached cell and removing the suspension cell). DCs were then generated by culturing PBMCs for six days with 30 ng/ml recombinant human granulocyte-macrophage stimulating factor (rhGM-CSF) and 20 ng/ml recombinant human interleukin-4 (rhIL-4) in vitro. On the sixth day, TNF-alpha (TNFalpha) 30 ng/ml was added into some DC cultures, which were then incubated for two additional days. The morphology was monitored by light microscopy and transmission electronic microscopy, and the phenotypes were determined by flow cytometry. Autologous mixed leukocyte reactions (MLR) were used to characterize DC function after TNFalpha or lipopolysaccharide (LPS) stimulations for 24 h. RESULTS: After six days of culture, the monocytes developed significant dendritic morphology and a portion of cells expressed CD1a, CD80 and CD86, features of DCs. TNFalpha treatment induced DCs maturation and up-regulation of CD80, CD86 and CD83. Autologous MLR demonstrated that these DCs possess potent T-cell stimulatory capacity. CONCLUSION: This study developed a simple and easy way to generate DCs from PBMCs exposed to rhGM-CSF and rhIL-4. The DCs produced by this method acquired morphologic and antigenic characteristics of DCs.

Cell Culture Techniques↗
PubMed2005

[Lipopolysaccharide (LPS) increases tumor necrosis factor-alpha related apoptosis induced-ligand (TRAIL) in macrophages killing HepG2 cells].

OBJECTIVE: To investigate the influence of lipopolysaccharide (LPS) on macrophages expressing TNF-alpha related apoptosis induced-ligand (TRAIL) and its relation to apoptosis of HepG2 cell line. METHODS: Membrane-bound TRAIL (mTRAIL) was measured by flow cytometry; soluble TRAIL in supernatant was detected by enzyme-linked immunoabsorbent sandwich assay (ELISA); cytotoxicity of TRAIL to HepG2 cell line was measured by chromium release assay, and apoptosis of HepG2 cell was confirmed by Annexin V staining. RESULTS: LPS only slightly increased membrane-bound TRAIL expression of macrophages. On the other hand, soluble TRAIL in the supernatant was increased with LPS stimulation, and the optimal concentration of LPS was 100 ng/ml (sTRAIL value 67.40 ng/ml+/-5.08 ng/ml). The soluble TRAIL in the supernatant was cytotoxic to HepG2 cells, and this activity can be blocked by TRAIL neutralizing antibodies. CONCLUSION: LPS increases the expression of soluble TRAIL in macrophages, and soluble TRAIL is toxic to HepG2 cells. All of our results indicate that TRAIL may play an important role in the pathogenesis of viral hepatitis.

Apoptosis↗