心梗后大鼠心肌TNF-α表达与室性心律失常关系的研究
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摘要
目的：研究TNF-α在心梗后大鼠心室肌细胞中的表达特点及其在心梗后室性心律失常发生中的作用。
方法：将360只雄性SD大鼠随机分为假手术组(Sham组, n=120)、TNF-α螯合剂组（rhTNFR:Fc组, n=120）和心肌梗死组(MI组,n=120)3组，运用LAD结扎法建立大鼠心梗模型。在MI模型建立1d、3d、7d、14d、1m、2m后，分别运用程序电刺激方法，观察是否诱发室性心律失常。同时用激光共聚焦显微镜观察TNF-α蛋白在心室肌的分布情况，用Western Blot法检测心室肌TNF-α蛋白表达。
结果：与假手术组相比，各时间点心梗组大鼠程序电诱发的室性心律失常发生率率明显增高（P<0.05）；Western Blot检测的心室肌组织TNF-α表达明显增加（P<0.05），且随着心梗的病理进程TNF-α的表达逐渐增加，在14d达到峰值后逐渐降低；与心梗组相比，各时间点rhTNFR:Fc组大鼠程序电诱发的室性心律失常发生率率明显降低（P<0.05），Western Blot检测的心肌组织TNF-α表达显著减少（P<0.05）。
结论：与假手术组相比，心梗后大鼠心肌组织TNF-α表达明显增加，且随心梗的病理进程其表达增加，在14d达到峰值后逐渐降低；减少TNF-α的表达可以降低心梗后室性心律失常的发生率；大量TNF-α表达在心梗后室性心律失常的发生中发挥着重要作用。
目的：研究Cx43在心梗后大鼠心室肌细胞中的表达特点及其在心梗后室性心律失常发生中的作用。
方法：将240只雄性SD大鼠随机分为假手术组(Sham组, n=120)和心肌梗死组(MI组,n=120)2组，运用LAD结扎法建立大鼠心梗模型。在MI模型建立1d、3d、7d、14d、1m、2m后，分别运用程序电刺激方法，观察是否诱发室性心律失常。同时用激光共聚焦显微镜观察Cx43蛋白在心室肌的分布情况，用Western Blot法检测心室肌非磷酸化Cx43和磷酸化Cx43蛋白表达。
结果：与假手术组相比，各时间点心梗组大鼠程序电诱发的室性心律失常发生率率明显增高（P<0.05）；Western Blot检测的心室肌组织非磷酸化Cx43表达显著增加（P<0.05），磷酸化Cx43表达显著降低（P<0.05），且随着心梗的病理进程Cx43的表达逐渐变化，在14d变化最显著并在其后稳定存在。激光共聚焦显微镜观察显示，假手术组Cx43在心室肌细胞上分布较有序，主要分布在闰盘处；心梗组Cx43在心室肌细胞上分布紊乱，主要在心室肌细胞间侧对侧分布；此种异常分布也在心梗后14d最为显著。
结论：心梗后大鼠心室肌组织Cx43出现非磷酸化重构，在心室肌细胞上的分布出现异常，且随心梗的病理进程其表达增加，在14d达到峰值，并在其后稳定存在；Cx43的表达和分布异常与心梗后室性心律失常的发生密切相关。
目的：研究TNF-α对大鼠心肌梗死后Cx43的调节作用及其对心肌梗死后室性心律失常发生的影响。
方法：将360只雄性SD大鼠随机分为假手术组(Sham组, n=120)、TNF-α螯合剂组（rhTNFR:Fc组, n=120）和心肌梗死组(MI组,n=120)3组，运用LAD结扎法建立大鼠心梗模型。在MI模型建立1d、3d、7d、14d、1m、2m后，分别运用程序电刺激方法，观察是否诱发室性心律失常。同时用激光共聚焦显微镜观察TNF-α和Cx43蛋白在心室肌的分布情况，用Western Blot法检测心室肌TNF-α、非磷酸化Cx43以及磷酸化Cx43蛋白表达。
结果：与假手术组相比，各时间点心梗组大鼠程序电诱发的室性心律失常发生率率明显增高（P<0.05）；Western Blot检测的心室肌组织TNF-α表达明显增加（P<0.05），非磷酸化Cx43表达显著增加（P<0.05），磷酸化Cx43表达显著降低（P<0.05）且随着心梗的病理进程TNF-α、非磷酸化Cx43、磷酸化Cx43的表达逐渐变化，在14d达到峰值后TNF-α的表达逐渐降低，而非磷酸化Cx43、磷酸化Cx43的表达在其后稳定存在；激光共聚焦显微镜观察显示，假手术组Cx43在心室肌细胞上分布较有序，主要分布在闰盘处；心梗组Cx43在心室肌细胞上分布紊乱，主要在心室肌细胞间侧对侧分布；此种异常分布也在心梗后14d最为显著。与心梗组相比，各时间点rhTNFR:Fc组大鼠程序电诱发的室性心律失常发生率率明显降低（P<0.05），Western Blot检测的心室肌组织TNF-α表达显著减少（P<0.05），非磷酸化Cx43表达显著增加（P<0.05），磷酸化Cx43表达显著降低（P<0.05）；激光共聚焦显微镜观察显示Cx43的分布紊乱有改善，在心室肌细胞间主要呈端对端分布。
结论：心梗后，心室肌细胞中高表达的TNF-α可以诱导Cx43非磷酸化重构和分布异常，从而在心梗后室性心律失常的发生中发挥重要作用。
Objective： To study TNF-α expression in cardiomyocytes of rats after myocardialinfarction and its role on ventricular arrhythmias after myocardial infarction.
Methods：360male SD rats were randomly divided into control group, rhTNFR: Fc group,and myocardial infarction group. By ligation the left anterior descending (LAD) ofcoronary artery of rats we established the rat myocardial infarction model. Then weobserved whether ventricular arrhythmia could be induced by programmed electricalstimulation1day,3days,7days,14days,1month and2months after MI. The expressionof TNF-α was also examined by western blot and laser scanning confocal at the same timepoint.
Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of TNF-α increased gradually after myocardial infarction, reaching the peak in14days after MI, then the expression reduced gradually. Compared with MI group, theincidence rate of induced ventricular arrhythmia by program electric was decreasedsignificantly (P <0.05) in rhTNFR:Fc group at each time point,, The result of Western Blotshowed TNF-α expression reduced significantly (P <0.05) as well.
Conclusion：The expression of TNF-α increased significantly after myocardial infarction.The incidence rate of induced ventricular arrhythmia by program electric increasedsignificantly. Lowering the expression of TNF-α could reduce induced ventriculararrhythmia. TNF-α may play an important role in the occurrence of ventricular arrhythmiaafter myocardial infarction.
Objective：To study Cx43expression in cardiomyocytes of rats after myocardial infarctionand its role on ventricular arrhythmias after myocardial infarction.
Methods：240male SD rats were randomly divided into control group and myocardialinfarction group. By ligation the left anterior descending (LAD) of coronary artery of ratswe established the rat myocardial infarction model. Then we observed whether ventriculararrhythmia could be induced by programmed electrical stimulation1day,3days,7days,14days,1month and2months after MI. The expression of Cx43was also examined bywestern blot and laser scanning confocal at the same time point.
Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of nonphoshporylated Cx43increased and the expression of phoshporylatedCx43decreased after myocardial infarction. The abnormal expression and distribution ofCx43changed gradually after myocardial infarction, reaching the peak in14days after MI,being stable from then on.
Conclusion：Cx43may play an important role in the occurrence of ventricular arrhythmiaafter myocardial infarction.
Objective: To study the relationship of TNF-α on regulation of Cx43and ventriculararrhythmias after myocardial infarction in rats.
Methods:360male SD rats were randomly divided into control group, rhTNFR: Fc group,and myocardial infarction group. By ligation the left anterior descending (LAD) ofcoronary artery of rats we established the rat myocardial infarction model. Then weobserved whether ventricular arrhythmia could be induced by programmed electricalstimulation1day,3days,7days,14days,1month and2months after MI. The expressionof TNF-α and Cx43was also examined by western blot and laser scanning confocal at thesame time point.
Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of TNF-α increased gradually after myocardial infarction; The expression ofnonphoshporylated Cx43increased and the expression of phoshporylated Cx43decreasedafter myocardial infarction. These change reached the peak in14days after MI, and theabnormal was stable from then on. Compared with MI group, the incidence rate of inducedventricular arrhythmia by program electric was increased significantly (P <0.05) inrhTNFR:Fc group at each time point. The result of Western Blot showed TNF-α expressionreduced significantly (P <0.05) as well.
Conclusion: The high expression of TNF-α can induce the nonphosphorylated refactoringand abnormal distribution of Cx43, thus play an important role in the occurrence ofventricular arrhythmia after myocardial infarction.
方法：将360只雄性SD大鼠随机分为假手术组(Sham组, n=120)、TNF-α螯合剂组（rhTNFR:Fc组, n=120）和心肌梗死组(MI组,n=120)3组，运用LAD结扎法建立大鼠心梗模型。在MI模型建立1d、3d、7d、14d、1m、2m后，分别运用程序电刺激方法，观察是否诱发室性心律失常。同时用激光共聚焦显微镜观察TNF-α蛋白在心室肌的分布情况，用Western Blot法检测心室肌TNF-α蛋白表达。
结果：与假手术组相比，各时间点心梗组大鼠程序电诱发的室性心律失常发生率率明显增高（P<0.05）；Western Blot检测的心室肌组织TNF-α表达明显增加（P<0.05），且随着心梗的病理进程TNF-α的表达逐渐增加，在14d达到峰值后逐渐降低；与心梗组相比，各时间点rhTNFR:Fc组大鼠程序电诱发的室性心律失常发生率率明显降低（P<0.05），Western Blot检测的心肌组织TNF-α表达显著减少（P<0.05）。
结论：与假手术组相比，心梗后大鼠心肌组织TNF-α表达明显增加，且随心梗的病理进程其表达增加，在14d达到峰值后逐渐降低；减少TNF-α的表达可以降低心梗后室性心律失常的发生率；大量TNF-α表达在心梗后室性心律失常的发生中发挥着重要作用。
目的：研究Cx43在心梗后大鼠心室肌细胞中的表达特点及其在心梗后室性心律失常发生中的作用。
方法：将240只雄性SD大鼠随机分为假手术组(Sham组, n=120)和心肌梗死组(MI组,n=120)2组，运用LAD结扎法建立大鼠心梗模型。在MI模型建立1d、3d、7d、14d、1m、2m后，分别运用程序电刺激方法，观察是否诱发室性心律失常。同时用激光共聚焦显微镜观察Cx43蛋白在心室肌的分布情况，用Western Blot法检测心室肌非磷酸化Cx43和磷酸化Cx43蛋白表达。
结果：与假手术组相比，各时间点心梗组大鼠程序电诱发的室性心律失常发生率率明显增高（P<0.05）；Western Blot检测的心室肌组织非磷酸化Cx43表达显著增加（P<0.05），磷酸化Cx43表达显著降低（P<0.05），且随着心梗的病理进程Cx43的表达逐渐变化，在14d变化最显著并在其后稳定存在。激光共聚焦显微镜观察显示，假手术组Cx43在心室肌细胞上分布较有序，主要分布在闰盘处；心梗组Cx43在心室肌细胞上分布紊乱，主要在心室肌细胞间侧对侧分布；此种异常分布也在心梗后14d最为显著。
结论：心梗后大鼠心室肌组织Cx43出现非磷酸化重构，在心室肌细胞上的分布出现异常，且随心梗的病理进程其表达增加，在14d达到峰值，并在其后稳定存在；Cx43的表达和分布异常与心梗后室性心律失常的发生密切相关。
目的：研究TNF-α对大鼠心肌梗死后Cx43的调节作用及其对心肌梗死后室性心律失常发生的影响。
方法：将360只雄性SD大鼠随机分为假手术组(Sham组, n=120)、TNF-α螯合剂组（rhTNFR:Fc组, n=120）和心肌梗死组(MI组,n=120)3组，运用LAD结扎法建立大鼠心梗模型。在MI模型建立1d、3d、7d、14d、1m、2m后，分别运用程序电刺激方法，观察是否诱发室性心律失常。同时用激光共聚焦显微镜观察TNF-α和Cx43蛋白在心室肌的分布情况，用Western Blot法检测心室肌TNF-α、非磷酸化Cx43以及磷酸化Cx43蛋白表达。
结果：与假手术组相比，各时间点心梗组大鼠程序电诱发的室性心律失常发生率率明显增高（P<0.05）；Western Blot检测的心室肌组织TNF-α表达明显增加（P<0.05），非磷酸化Cx43表达显著增加（P<0.05），磷酸化Cx43表达显著降低（P<0.05）且随着心梗的病理进程TNF-α、非磷酸化Cx43、磷酸化Cx43的表达逐渐变化，在14d达到峰值后TNF-α的表达逐渐降低，而非磷酸化Cx43、磷酸化Cx43的表达在其后稳定存在；激光共聚焦显微镜观察显示，假手术组Cx43在心室肌细胞上分布较有序，主要分布在闰盘处；心梗组Cx43在心室肌细胞上分布紊乱，主要在心室肌细胞间侧对侧分布；此种异常分布也在心梗后14d最为显著。与心梗组相比，各时间点rhTNFR:Fc组大鼠程序电诱发的室性心律失常发生率率明显降低（P<0.05），Western Blot检测的心室肌组织TNF-α表达显著减少（P<0.05），非磷酸化Cx43表达显著增加（P<0.05），磷酸化Cx43表达显著降低（P<0.05）；激光共聚焦显微镜观察显示Cx43的分布紊乱有改善，在心室肌细胞间主要呈端对端分布。
结论：心梗后，心室肌细胞中高表达的TNF-α可以诱导Cx43非磷酸化重构和分布异常，从而在心梗后室性心律失常的发生中发挥重要作用。
Objective： To study TNF-α expression in cardiomyocytes of rats after myocardialinfarction and its role on ventricular arrhythmias after myocardial infarction.
Methods：360male SD rats were randomly divided into control group, rhTNFR: Fc group,and myocardial infarction group. By ligation the left anterior descending (LAD) ofcoronary artery of rats we established the rat myocardial infarction model. Then weobserved whether ventricular arrhythmia could be induced by programmed electricalstimulation1day,3days,7days,14days,1month and2months after MI. The expressionof TNF-α was also examined by western blot and laser scanning confocal at the same timepoint.
Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of TNF-α increased gradually after myocardial infarction, reaching the peak in14days after MI, then the expression reduced gradually. Compared with MI group, theincidence rate of induced ventricular arrhythmia by program electric was decreasedsignificantly (P <0.05) in rhTNFR:Fc group at each time point,, The result of Western Blotshowed TNF-α expression reduced significantly (P <0.05) as well.
Conclusion：The expression of TNF-α increased significantly after myocardial infarction.The incidence rate of induced ventricular arrhythmia by program electric increasedsignificantly. Lowering the expression of TNF-α could reduce induced ventriculararrhythmia. TNF-α may play an important role in the occurrence of ventricular arrhythmiaafter myocardial infarction.
Objective：To study Cx43expression in cardiomyocytes of rats after myocardial infarctionand its role on ventricular arrhythmias after myocardial infarction.
Methods：240male SD rats were randomly divided into control group and myocardialinfarction group. By ligation the left anterior descending (LAD) of coronary artery of ratswe established the rat myocardial infarction model. Then we observed whether ventriculararrhythmia could be induced by programmed electrical stimulation1day,3days,7days,14days,1month and2months after MI. The expression of Cx43was also examined bywestern blot and laser scanning confocal at the same time point.
Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of nonphoshporylated Cx43increased and the expression of phoshporylatedCx43decreased after myocardial infarction. The abnormal expression and distribution ofCx43changed gradually after myocardial infarction, reaching the peak in14days after MI,being stable from then on.
Conclusion：Cx43may play an important role in the occurrence of ventricular arrhythmiaafter myocardial infarction.
Objective: To study the relationship of TNF-α on regulation of Cx43and ventriculararrhythmias after myocardial infarction in rats.
Methods:360male SD rats were randomly divided into control group, rhTNFR: Fc group,and myocardial infarction group. By ligation the left anterior descending (LAD) ofcoronary artery of rats we established the rat myocardial infarction model. Then weobserved whether ventricular arrhythmia could be induced by programmed electricalstimulation1day,3days,7days,14days,1month and2months after MI. The expressionof TNF-α and Cx43was also examined by western blot and laser scanning confocal at thesame time point.
Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of TNF-α increased gradually after myocardial infarction; The expression ofnonphoshporylated Cx43increased and the expression of phoshporylated Cx43decreasedafter myocardial infarction. These change reached the peak in14days after MI, and theabnormal was stable from then on. Compared with MI group, the incidence rate of inducedventricular arrhythmia by program electric was increased significantly (P <0.05) inrhTNFR:Fc group at each time point. The result of Western Blot showed TNF-α expressionreduced significantly (P <0.05) as well.
Conclusion: The high expression of TNF-α can induce the nonphosphorylated refactoringand abnormal distribution of Cx43, thus play an important role in the occurrence ofventricular arrhythmia after myocardial infarction.
引文
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19. Même W, Calvo CF, Froger N. Proinflammatory cytokines released from microgliainhibit gap junctions in astrocytes: potentiation by beta-amyloid. FASEB J,2006,20(3):494-496.
1.高润霖,陈在嘉.冠心病.北京:人民卫生出版社,2001.338-339.
2. Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias.N Engl J Med,2001,345(20):1473-1482.
3. Zha JK, Shu HB. Molecular mechanism of signaling by tumor necrosis factor. SciChina C Life Sci,2002,45(2):113-118.
4. Bazzoni F, Beutler B. How do tumor necrosis fator receptor work? J Inflamm,1995,45(4):221-238.
5. Sack M. Tumor necrosis factor-alpha in cardiovascular biology and the potentialrole for anti-tumor necrosis factor-alpha therapy in heart disease. Pharmacol Ther,2002,94(122):123-126.
6. Wada H, Saito K, Kobayashi I et al.Tumor Necrosis Factor-α Plays a ProtectiveRole in Acute Viral Myocarditis in Mice. Circulation,2001,103:743-749.
7. Mann D, Mcmurray JV, Packer M et al. Targeted anticytokine therapy in patientswith chronic heart failure. Circulation,2004,109:1594-1602.
8. Kubica J, Kozinski M, Krzewina-Kowalska A, et al. Combined periproceduralevaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis andmajor adverse cardiac events in patients undergoing percutaneous coronaryinterventions. Int J Mol Med,2005,16(1):173-180.
9. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response inmyocardial infarction. Cardiovasc Res,2002,53(1):31-47.
10. Alexander RW.Inflammation and Coronary Artery Disease. N Engl J Med,1994,331(7):468-469.
11. Jacobs M, Staufenberger S, Gergs U, et al. Tumor necrosis factor-alpha at acutemyocardial infarction in rats and effects on cardiac fibroblasts. J Mol Cell Cardiol,1999,31(11):1949-1959.
12.肖华，陈志坚，廖玉华，等. TNF-α早期表达在大鼠急性心肌梗死室性心律失常发生中的作用及机制研究.中国免疫学杂志,2008,24(1):75-78.
13.陈昱,陈志坚,曹喆,等.重组人肿瘤坏死因子受体融合蛋白对大鼠急性心肌梗死室性心律失常的影响.临床心血管病杂志,2009,25(8):585-587.
14. Ono K, Matsumori A, Shioi T, et al. Cytokine Gene Expression After MyocardialInfarction in Rat Hearts: Possible Implication in Left Ventricular Remodeling.Circulation,1998,98:149-156.
15. Bradham WS, Bozkurt B, Gunasinghe H, et al. Tumor necrosis factor-alpha andmyocardial remodeling in progression of heart failure: a current perspective.Cardiovasc Res,2002,53(4):822-830.
16. Xiao H, Chen Z, Liao Y, et al. Positive correlation of tumor necrosis factor-alphaearly expression in myocardium and ventricular arrhythmias in rats with acutemyocardial infarction. Arch Med Res,2008,39(3):285-291.
17. Shimoda Y, Satoh M, Nakamura M, et al. Activated tumour necrosisfactor-shedding process is associated with in-hospital complication in patients withacute myocardial infarction. Clinical Science,2005,108:339–347.
18. Petkova-Kirova PS, Gursoy E, Mehdi H, et al. Electrical remodeling of cardiacmyocytes from mice with heart failure due to the overexpression of tumor necrosisfactor-α. Am J Physiol Heart Circ Physiol,2006,290: H2098–H2107.
19.曹喆,陈志坚,陈昱,等. RhTNFR:Fc体外大鼠心脏心肌梗死后快速心律失常影响的研究.临床心血管病杂志,2009,25(3):182-184.
20. Yu Y, Huang M, Li WD, et al. Therapeutic effects of rhu-TNFR-Fc on adjuvantarthritis and its possible mechanism in rats. J Chin Pharm,2004,39:435-438.
1.高润霖,陈在嘉.冠心病.北京:人民卫生出版社,2001.338-339.
2. Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias.N Engl J Med,2001,345(20):1473-1482.
3. Zha JK, Shu HB. Molecular mechanism of signaling by tumor necrosis factor. SciChina C Life Sci,2002,45(2):113-118.
4. Bazzoni F, Beutler B. How do tumor necrosis fator receptor work? J Inflamm,1995,45(4):221-238.
5. Sack M. Tumor necrosis factor-alpha in cardiovascular biology and the potentialrole for anti-tumor necrosis factor-alpha therapy in heart disease. Pharmacol Ther,2002,94(122):123-126.
6. Wada H, Saito K, Kobayashi I et al.Tumor Necrosis Factor-α Plays a ProtectiveRole in Acute Viral Myocarditis in Mice. Circulation,2001,103:743-749.
7. Mann D, Mcmurray JV, Packer M et al. Targeted anticytokine therapy in patientswith chronic heart failure. Circulation,2004,109:1594-1602.
8. Kubica J, Kozinski M, Krzewina-Kowalska A, et al. Combined periproceduralevaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis andmajor adverse cardiac events in patients undergoing percutaneous coronaryinterventions. Int J Mol Med,2005,16(1):173-180.
9. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response inmyocardial infarction. Cardiovasc Res,2002,53(1):31-47.
10. Alexander RW.Inflammation and Coronary Artery Disease. N Engl J Med,1994,331(7):468-469.
11. Jacobs M, Staufenberger S, Gergs U, et al. Tumor necrosis factor-alpha at acutemyocardial infarction in rats and effects on cardiac fibroblasts. J Mol Cell Cardiol,1999,31(11):1949-1959.
12.肖华，陈志坚，廖玉华，等. TNF-α早期表达在大鼠急性心肌梗死室性心律失常发生中的作用及机制研究.中国免疫学杂志,2008,24(1):75-78.
13.陈昱,陈志坚,曹喆,等.重组人肿瘤坏死因子受体融合蛋白对大鼠急性心肌梗死室性心律失常的影响.临床心血管病杂志,2009,25(8):585-587.
14. Ono K, Matsumori A, Shioi T, et al. Cytokine Gene Expression After MyocardialInfarction in Rat Hearts: Possible Implication in Left Ventricular Remodeling.Circulation,1998,98:149-156.
15. Bradham WS, Bozkurt B, Gunasinghe H, et al. Tumor necrosis factor-alpha andmyocardial remodeling in progression of heart failure: a current perspective.Cardiovasc Res,2002,53(4):822-830.
16. Xiao H, Chen Z, Liao Y, et al. Positive correlation of tumor necrosis factor-alphaearly expression in myocardium and ventricular arrhythmias in rats with acutemyocardial infarction. Arch Med Res,2008,39(3):285-291.
17. Shimoda Y, Satoh M, Nakamura M, et al. Activated tumour necrosisfactor-shedding process is associated with in-hospital complication in patients withacute myocardial infarction. Clinical Science,2005,108:339–347.
18. Petkova-Kirova PS, Gursoy E, Mehdi H, et al. Electrical remodeling of cardiacmyocytes from mice with heart failure due to the overexpression of tumor necrosisfactor-α. Am J Physiol Heart Circ Physiol,2006,290: H2098–H2107.
19.曹喆,陈志坚,陈昱,等. RhTNFR:Fc体外大鼠心脏心肌梗死后快速心律失常影响的研究.临床心血管病杂志,2009,25(3):182-184.
20. Yu Y, Huang M, Li WD, et al. Therapeutic effects of rhu-TNFR-Fc on adjuvantarthritis and its possible mechanism in rats. J Chin Pharm,2004,39:435-438.
1. Myerburg RJ, Castellanos A. Cardiac arrest and sudden cardiac death. In: Libby P,Bonow RO, Mann DL, Zipes DP (eds): Braunwald’s Heart Disease: A Textbook ofCardiovascular Medicine,8th ed. Philadelphia: WB Saunders,2008.933-974.
2. Antman EM, Braunwald E. ST-Elevation Myocardiol Infarction: Pathology,Pathophysiology, and Clinical Features. In: Libby P, Bonow RO, Mann DL, ZipesDP (eds): Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine,8thed. Philadelphia: WB Saunders,2008.1207-1232.
3. Callans DJ, Josepbson ME. Ventricular Tachycardia in Patients with CoronaryArtery Disease.In: Zipes DP, Jalife J (eds): Cardiac Electrophysiology: From Cellto Bedside,4th ed. Philadelphia: WB Saunders,2004.569-574.
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8. Peters NS, Coromilas J, Severs NJ, et al. Disturbed Connexin43Gap JunctionDistribution Correlates With the Location of Reentrant Circuits in the EpicardialBorder Zone of Healing Canine Infarcts That Cause Ventricular Tachycardia.Circulation,1997,95:988-996.
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10. Roell W, Lewalter T, Sasse P, et al. Engraftment of connexin43-expressing cellsprevents post-infarct arrhythmia. Nature,2007,450:819-824.
11. Tselentakis EV, Woodford E, Chandy J, et al. Inflammation effects on the electricalproperties of atrial tissue and inducibility of postoperative atrial fibrillation. J SurgRes,2006,135(1):68-75.
12.肖华，陈志坚，廖玉华，等.大鼠心肌梗死后肿瘤坏死因子-α的早期表达与室性心律失常的关系研究.医学临床研究,2007,24(1):6-9.
13. Herskowitz A, Choi S, Ansari AA, et al. Cytokine mRNA expression inpostischemic/reperfused myocardium. Am J Pathol,1995,146(2):419-428.
14. Ono K, Matsumori A, Shioi T, et al. Cytokine Gene Expression After MyocardialInfarction in Rat Hearts: Possible Implication in Left Ventricular Remodeling.Circulation,1998,98:149-156.
15.陈志坚,廖玉华,肖华,等.鼠巨细胞病毒心肌炎自身免疫致室性心律失常机制的研究.临床心血管病杂志,2007,23(1):55-58.
16.肖华,陈志坚,廖玉华,等.急性心肌梗死肿瘤坏死因子-α表达与室性心律失常的关系研究.中华急诊医学杂志,2008,17(12):1292-1295.
17. Shimoda Y, Satoh M, Nakamura M, et al. Activated tumour necrosis factor-αshedding process is associated with in-hospital complication in patients with acutemyocardial infarction. Clinical Science,2005,108:339–347.
18.肖华,陈志坚,廖玉华,等.肿瘤坏死因子-α致室性心律失常作用的研究.临床心血管病杂志,2007,23(2):141-143.
19. Petkova-Kirova PS, Gursoy E, Mehdi H, et al. Electrical remodeling of cardiacmyocytes from mice with heart failure due to the overexpression of tumor necrosisfactor-α. Am J Physiol Heart Circ Physiol,2006,290:H2098–H2107.
20.曹喆,陈志坚,陈昱,等. rhTNFR:Fc对体外大鼠心脏心肌梗死后快速心律失常影响的研究.临床心血管病杂志,2009,25(3):182-184.
21. Eugenín EA, Bra es MC, Berman JW, et al. TNF-alpha plus IFN-gamma induceconnexin43expression and formation of gap junctions between humanmonocytes/macrophages that enhance physiological responses. J Immunol,2003,170(3):1320-1328.
22. Sharrow AC, Li Y, Micsenyi A, et al. Modulation of osteoblast gap junctionconnectivity by serum, TNFalpha, and TRAIL. Exp Cell Res,2008,314(2):297-308.
23. Wang M, Berthoud VM, Beyer EC. Connexin43increases the sensitivity of prostatecancer cells to TNFalpha-induced apoptosis. J Cell Sci,2007,120(2):320-329.
24. Même W, Calvo CF, Froger N. Proinflammatory cytokines released from microgliainhibit gap junctions in astrocytes: potentiation by beta-amyloid. FASEB J,2006,20(3):494-496.
25. Sawaya SE, Rajawat YS, Rami TG, et al. Downregulation of connexin40andincreased prevalence of atrial arrhythmias in transgenic mice with cardiac-restrictedoverexpression of tumor necrosis factor. Am J Physiol Heart Circ Physiol,2007,292:H1561–H1567.
26. Salameh A, Schneider P, Mqhlberg K, et al. Chronic regulation of the expression ofgap junction proteins connexin40, connexin43, and connexin45in neonatal ratcardiomyocytes. European Journal of Pharmacology,2004,503:9-16.
27. Severs NJ, Dupont E, Coppen SR, et al.Remodelling of gap junctions and connexinexpression in heart disease. Biochim Biophys Acta,2004,1662(1-2):138-148.
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2. Antman EM, Braunwald E. ST-Elevation Myocardiol Infarction: Pathology,Pathophysiology, and Clinical Features. In: Libby P, Bonow RO, Mann DL, ZipesDP (eds): Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine,8thed. Philadelphia: WB Saunders,2008.1207-1232.
3. Callans DJ, Josepbson ME. Ventricular Tachycardia in Patients with CoronaryArtery Disease.In: Zipes DP, Jalife J (eds): Cardiac Electrophysiology: From Cellto Bedside,4th ed. Philadelphia: WB Saunders,2004.569-574.
4. Peters NS, Coromilas J, Severs NJ, et al. Disturbed Connexin43Gap JunctionDistribution Correlates With the Location of Reentrant Circuits in the EpicardialBorder Zone of Healing Canine Infarcts That Cause Ventricular Tachycardia.Circulation,1997,95:988-996.
5. Roell W, Lewalter T, Sasse P, et al. Engraftment of connexin43-expressing cellsprevents post-infarct arrhythmia. Nature,2007,450:819-824.
6. Tselentakis EV, Woodford E, Chandy J, et al. Inflammation effects on the electricalproperties of atrial tissue and inducibility of postoperative atrial fibrillation. J SurgRes,2006,135(1):68-75.
7.肖华，陈志坚，廖玉华，等.大鼠心肌梗死后肿瘤坏死因子-α的早期表达与室性心律失常的关系研究.医学临床研究,2007,24(1):6-9.
8. Herskowitz A, Choi S, Ansari AA, et al. Cytokine mRNA expression inpostischemic/reperfused myocardium. Am J Pathol,1995,146(2):419-428.
9. Ono K, Matsumori A, Shioi T, et al. Cytokine Gene Expression After MyocardialInfarction in Rat Hearts: Possible Implication in Left Ventricular Remodeling.Circulation,1998,98:149-156.
10.陈志坚,廖玉华,肖华,等.鼠巨细胞病毒心肌炎自身免疫致室性心律失常机制的研究.临床心血管病杂志,2007,23(1):55-58.
11.肖华,陈志坚,廖玉华,等.急性心肌梗死肿瘤坏死因子-α表达与室性心律失常的关系研究.中华急诊医学杂志,2008,17(12):1292-1295.
12. Shimoda Y, Satoh M, Nakamura M, et al. Activated tumour necrosis factor-αshedding process is associated with in-hospital complication in patients with acutemyocardial infarction. Clinical Science,2005,108:339–347.
13.肖华,陈志坚,廖玉华,等.肿瘤坏死因子-α致室性心律失常作用的研究.临床心血管病杂志,2007,23(2):141-143.
14. Petkova-Kirova PS, Gursoy E, Mehdi H, et al. Electrical remodeling of cardiacmyocytes from mice with heart failure due to the overexpression of tumor necrosisfactor-α. Am J Physiol Heart Circ Physiol,2006,290: H2098–H2107.
15.曹喆,陈志坚,陈昱,等. rhTNFR: Fc对体外大鼠心脏心肌梗死后快速心律失常影响的研究.临床心血管病杂志,2009,25(3):182-184.
16. Eugenín EA, Bra es MC, Berman JW, et al. TNF-alpha plus IFN-gamma induceconnexin43expression and formation of gap junctions between human monocytes/macrophages that enhance physiological responses. J Immunol,2003,170(3):1320-1328.
17. Sharrow AC, Li Y, Micsenyi A, et al. Modulation of osteoblast gap junctionconnectivity by serum, TNFalpha, and TRAIL. Exp Cell Res,2008,314(2):297-308.
18. Wang M, Berthoud VM, Beyer EC. Connexin43increases the sensitivity of prostatecancer cells to TNFalpha-induced apoptosis. J Cell Sci,2007,120(2):320-329.
19. Même W, Calvo CF, Froger N. Proinflammatory cytokines released from microgliainhibit gap junctions in astrocytes: potentiation by beta-amyloid. FASEB J,2006,20(3):494-496.
1.高润霖,陈在嘉.冠心病.北京:人民卫生出版社,2001.338-339.
2. Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias.N Engl J Med,2001,345(20):1473-1482.
3. Zha JK, Shu HB. Molecular mechanism of signaling by tumor necrosis factor. SciChina C Life Sci,2002,45(2):113-118.
4. Bazzoni F, Beutler B. How do tumor necrosis fator receptor work? J Inflamm,1995,45(4):221-238.
5. Sack M. Tumor necrosis factor-alpha in cardiovascular biology and the potentialrole for anti-tumor necrosis factor-alpha therapy in heart disease. Pharmacol Ther,2002,94(122):123-126.
6. Wada H, Saito K, Kobayashi I et al.Tumor Necrosis Factor-α Plays a ProtectiveRole in Acute Viral Myocarditis in Mice. Circulation,2001,103:743-749.
7. Mann D, Mcmurray JV, Packer M et al. Targeted anticytokine therapy in patientswith chronic heart failure. Circulation,2004,109:1594-1602.
8. Kubica J, Kozinski M, Krzewina-Kowalska A, et al. Combined periproceduralevaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis andmajor adverse cardiac events in patients undergoing percutaneous coronaryinterventions. Int J Mol Med,2005,16(1):173-180.
9. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response inmyocardial infarction. Cardiovasc Res,2002,53(1):31-47.
10. Alexander RW.Inflammation and Coronary Artery Disease. N Engl J Med,1994,331(7):468-469.
11. Jacobs M, Staufenberger S, Gergs U, et al. Tumor necrosis factor-alpha at acutemyocardial infarction in rats and effects on cardiac fibroblasts. J Mol Cell Cardiol,1999,31(11):1949-1959.
12.肖华，陈志坚，廖玉华，等. TNF-α早期表达在大鼠急性心肌梗死室性心律失常发生中的作用及机制研究.中国免疫学杂志,2008,24(1):75-78.
13.陈昱,陈志坚,曹喆,等.重组人肿瘤坏死因子受体融合蛋白对大鼠急性心肌梗死室性心律失常的影响.临床心血管病杂志,2009,25(8):585-587.
14. Ono K, Matsumori A, Shioi T, et al. Cytokine Gene Expression After MyocardialInfarction in Rat Hearts: Possible Implication in Left Ventricular Remodeling.Circulation,1998,98:149-156.
15. Bradham WS, Bozkurt B, Gunasinghe H, et al. Tumor necrosis factor-alpha andmyocardial remodeling in progression of heart failure: a current perspective.Cardiovasc Res,2002,53(4):822-830.
16. Xiao H, Chen Z, Liao Y, et al. Positive correlation of tumor necrosis factor-alphaearly expression in myocardium and ventricular arrhythmias in rats with acutemyocardial infarction. Arch Med Res,2008,39(3):285-291.
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18. Petkova-Kirova PS, Gursoy E, Mehdi H, et al. Electrical remodeling of cardiacmyocytes from mice with heart failure due to the overexpression of tumor necrosisfactor-α. Am J Physiol Heart Circ Physiol,2006,290: H2098–H2107.
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