Fusheng Zhan

Publications (2)0 Total impact

• Article: [Experimental study on influence of ischemia-reperfusion on expression of hyperpolarization activated cyclic nucleotide gated cation channel 4 of sinoatrial node cells in rabbits in vivo].

  Yong Fu, Bin Liao, Fengxu Yu, Mingbin Deng, Zhiqiang Feng, Fusheng Zhan, Xin Li, Juyi Wan
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  ABSTRACT: To study the influence of ischemia-reperfusion on the expression of the hyperpolarization activated cyclic nucleotide gated cation channel 4 (HCN4) and to discuss the mechanism of functional disturbance of sinoatrial node tissue (SANT) after ischemia reperfusion injury (IRI). Eighty five healthy adult rabbits, weighing 2-3 kg, were randomly divided into 3 groups: control group [a suture passed under the root section of right coronary artery (RCA) without ligation, n=5], experimental group A (occluding the root section of RCA for 30 minutes, then loosening the root 2, 4, 8 and 16 hours, n=10), experimental group B (occluding the root section of RCA for 1 hour, then loosening the root 2, 4, 8 and 16 hours, n=10). At the end of the reperfusion, the SANT was cut off to do histopathological, transmission electron microscopical and immunohistochemical examinations and semi-quantitative analysis. The result of HE staining showed that patho-injure of sinoatrial node cell (SANC) happened in experimental groups A and B after 2 hours of reperfusion, the longer the reperfusion time was, the more serious patho-injure of SANC was after 4 and 8 hours of reperfusion, SANC reached peak of damage after 8 to 16 hours of reperfusion; patho-injure of SANC was more serious in experimental group B than in experimental group A at the same reperfusion time. Immunohistochemical staining showed that the expression of HCN4 located in cellular membrane and cytoplasm in the central area of SANC and gradually decreased from the center to borderline. The integral absorbance values of HCN4 expression in the control group (397.40 +/- 34.11) was significantly higher than those in the experimental group A (306.20 +/- 35.77, 216.60 +/- 18.59, 155.40 +/- 19.11 and 135.00 +/- 12.30) and in the experimental group B (253.70 +/- 35.66, 138.70 +/- 13.28, 79.10 +/- 9.60 and 69.20 +/- 8.42) after 2, 4, 8 and 16 hours of reperfusion (P < 0.05). With reperfusion time, the expression of HCN4 of SANC decreased, which was lowest after 8 hours of reperfusion; showing significant difference among 2, 4 and 8 hours after reperfusion (P < 0.05) and no significant difference between 8 and 16 hours after reperfusion (P > 0.05). At the same reperfusion time, the expression of HCN4 was higher in the experimental group A than in the experimental group B. The result of transmission electron microscope showed that ultramicrostructure of SANC was damaged after reperfusion in experimental groups A and B. The longer the reperfusion time was, the more serious ultramicrostructure damage of SANC was, and reached the peak of damage after 8 hours of reperfusion. Ultramicrostructure of SANC was not different between 8 and 16 hours of reperfusion. At the same reperfusion time, the ultramicrostructure damage of SANC was more serious in experimental group B than in experimental group A. IRI is harmful to the morphous and structure of SANC, and effects the expression of HCN4 of SANC, which is concerned with functional disturbance and arrhythmia.
  Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery 07/2009; 23(7):856-60.
• Article: [The role of the K+ channel in the inhibition of the human lung adenocarcinoma cell proliferation by rmhTNF].

  Zonglin Wang, Tianyang Dai, Fusheng Zhan, Xiaorong Zeng, Yan Yang
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  ABSTRACT: With the development of patch clamp and molecular biology technique, and the application of them in the investigation of tumor cellular membrane ion channnel, the ion channel is becoming the hot spot of the tumor base research gradually. The aim of this study is to investigate the electrophysiological properties of human lung adenocarcinoma cell line A-549 and the role of K+ channel in inhibition of cell proliferation by the recombinant mutant human tumor necrosis factor (rmhTNF). Ionic currents were recorded using the whole-cell patch clamp recording technique. The proliferation activity of A-549 cells was measured by MTT assay. The cell cycle and apoptosis rates of the carcinoma cells were measured by flow cytometric analysis (FCM). Whole-cell patch clamp recording revealed a voltage-gated K+ current in A-549 cells, which could be blocked by the K+ channel blocker, TEA and CsCl. The amplitude of K+ current was markedly diminished in all cells incubated with different concentration of rmhTNF (P < 0.01). Obvious inhibitive effect of rmhTNF on proliferation of the cells was found in vitro in a dose-dependent manner (P < 0.01), the maximal inhibitory rate was 38.68% when the concentration was 400U/mL. The rmhTNF inhibited the cell cycle shifting from G1 phase to S phase and promoted apoptosis as determined by FCM analysis. The proportion of G1 cells increased from 53.02% to 72.93%, and the apoptosis rate increased from 2.08% to 8.68%. The difference were significant between the control and the high concentration groups ( 200U/mL and 400U/mL) (P < 0.01). rmhTNF exerts its cytotoxic effects on A-549 cells through inhibiting cell cycle shifting and inducing apoptosis. The K+ channels on the A-549 cell membrane can be blocked by rmhTNF partly, and the effect of inhibiting proliferation and activating apoptosis on A-549 cells is a result of depression of the K+ channel.
  Zhongguo fei ai za zhi = Chinese journal of lung cancer 10/2006; 9(5):399-404.