M Feng

Yangzhou University, Chiang-tu, Jiangsu Sheng, China

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Publications (3)3.13 Total impact

  • Y Li · P-J Zhang · C Jin · B Zhou · X-Y Liu · L-D Tao · M Feng
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    ABSTRACT: Deferoxamine mesylate is known to ameliorate tissue ischemia-reperfusion injury. This study was designed to explore the impact of deferoxamine mesylate preconditioning (DMP) on pancreatic tissue and its possible effects during orthotopic liver autotransplantation. A modified orthotopic liver autotransplantation model was used to simulate pancreatic ischemia-reperfusion injury. Sprague-Dawley rats (0.25-0.30 kg) were randomly divided into normal control, autotransplantation (AT), systemic deferoxamine mesylate preconditioning (SDMP), and partial deferoxamine mesylate conditioning (PDMC) groups. The SDMP group was injected with deferoxamine mesylate (75-90 mg; 300 mg/kg), via the celiac artery at 24 and 48 hours before surgery. During surgery, the PDMC group underwent liver perfusion by means of deferoxamine mesylate solution (20 ml; 0.6 mmol/L) rather than Ringer's lactate solution, with no prior preconditioning. At 6, 24, and 48 hours after surgery, the rats were sacrificed to sample their pancreatic tissues for the expression of hypoxia-inducible factor-1α (HIF-1α) and malondialdehyde (MDA) content. The samples were subjected to blood chemistry analyses, light and transmission electron microscopic morphological studies, and quantitative measurement of HIF-1α expression. The serum levels of amylase, lipase, and MDA in SDMP and PDMC groups were significantly lower than those in the AT group at 6, 24, and 48 hours after orthotopic liver autotransplantation (P < .05). Light and electron microscopic analyses showed much more severe pancreatic injury in the autotransplantation than in the SDMP and PDMC groups. The HIF-1α expression was increased in the SDMP and PDMC groups more than in the autotransplantation group (P < .05). Deferoxamine mesylate preconditioning protected pancreatic tissue in orthotopic liver autotransplantation in rats. Inhibition of oxidative toxic reactions and up-regulated expression of HIF-1α protein are possible mechanisms.
    No preview · Article · Jun 2011 · Transplantation Proceedings
  • B Zhou · P-J Zhang · T Tian · C Jin · Y Li · M Feng · X-Y Liu · L Jie · L-D Tao
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    ABSTRACT: To investigate the effect on intrahepatic cholangiocytes mediated by hypoxic preconditioning (HP) after liver transplantation and the role of vascular endothelial growth factor (VEGF). This experiment was based on a model of rat orthotopic liver autotransplantation. Sprague-Dawley rats were randomly divided into 3 groups: normal control, autotransplantation (AT), and HP. The HP group was subjected to 8% oxygen atmosphere for 90 minutes before surgery. At 6, 12, 24, and 48 hours after autotransplantation, the rats were killed for testing .Serum total bilirubin, direct bilirubin, and alkaline phosphatase concentrations were determined. The microstructure of cholangiocytes and the ultramicrostructure of cholangioles were determined. Immunohistochemistry was used to detect the expression of VEGF and the proliferation rate of cholangiocytes. Total bilirubin, direct bilirubin, and alkaline phosphatase concentrations in the AT group increased considerably more than in the HP group during the entire interval (P < .05). Light microscopy demonstrated that the microstructure of cholangiocytes in the AT group was damaged more seriously than in the HP group. At transmission electron microscopy, the ultramicrostructure of cholangioles was changed more obviously than in the HP group. The expression of VEGF on cholangiocytes and the proliferation rate of cholangiocytes were higher in the HP group than in the AT group over the entire experiment (P < .05). Hypoxic preconditioning has a protective effect on cholangiocytes after liver autotransplantation. The mechanism may be related to HP-induced overexpression of VEGF on cholangiocytes.
    No preview · Article · Sep 2010 · Transplantation Proceedings
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    ABSTRACT: Hepatocyte apoptosis is a severe form of cell death after hepatic ischemia-reperfusion injury (HIRI), and its relief is an important issue in liver transplantation. Hypoxic preconditioning (HP) is considered to have protective effects on HIRI. This study was designed to explore the impact of HP on apoptosis and its possible mechanism during orthotopic liver autotransplantation. A modified orthotopic liver autotransplantation model was used to simulate HIRI. Sprague-Dawley rats were randomly divided into normal control, autotransplantation (AT) and HP groups. The HP group was subjected to an 8% oxygen atmosphere for 90 minutes before surgery. At 1, 6 and 24 hours after surgery, the rats were killed and their liver tissue was sampled to assess the expression of Bcl-2 protein. The samples were subjected to blood chemistry study, morphological study under a light or transmission electron microscope, and quantitative study of mitochondria. The serum levels of ALT and AST in the HP group were lower than those in the AT group at 1, 6 and 24 hours after orthotopic liver autotransplantation (P<0.05). Bcl-2 protein expression was increased in the HP group at each measurement point (P<0.05). Light microscopy showed that hepatic injury in the AT group was much more severe than in the HP group. Hepatocytes in the AT group showed typical apoptosis signs under a transmission electron microscope. The ultrastructural appearance of hepatocytes in the HP group was much better than in the AT group, and the area, perimeter and diameter of the mitochondria were smaller in the HP group than in the AT group (P<0.05). Hepatocytes sense and respond to decreased tissue oxygenation. Stimulation by HP relieves apoptosis by upregulating expression of Bcl-2 protein and its protection of mitochondria after orthotopic liver autotransplantation.
    Preview · Article · Feb 2009 · Hepatobiliary & pancreatic diseases international: HBPD INT