大鼠缺血性心肌损伤后早期抑制核因子κB对心肌修复的影响
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Effects of Inhibition of Nuclear Factor-κB in the Early Phase After Myocardial Ischemia on Myocardial Reparation in Rats
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    摘要:

    目的研究大鼠缺血性心肌损伤后早期抑制核因子κB对心肌修复及心功能的影响。方法应用大剂量异丙肾上腺素建立大鼠缺血性心肌损伤模型,造模后24h存活的大鼠随机分为实验组和治疗组,并设立对照组。治疗组给予大鼠腹腔注射100mg/kg吡咯烷二硫代氨基甲酸盐,每日1次,连续26d。检查心肌病理形态学、心肌核因子κB激活情况、心肌毛细血管密度及肌纤维母细胞浸润情况,并在实验第14、28天进行超声心动图检查观察心脏结构及心功能变化情况。结果实验组与治疗组心肌坏死面积无明显差异;应用吡咯烷二硫代氨基甲酸盐有效抑制了缺血性心肌损伤后心肌核因子κB的激活,并导致肉芽组织替代受损心肌组织延迟,心肌坏死边缘区毛细血管密度减低及心肌坏死区肌纤维母细胞浸润受抑制;治疗组室壁瘤的发生较实验组明显增加,实验第28天,治疗组心功能降低较实验组更为明显。结论大鼠缺血性心肌损伤后早期抑制核因子κB可能对心肌修复不利,并进而对心室重塑、心功能造成不良影响。

    Abstract:

    Aim To study the effects of inhibition of NF-κB in the early phase after myocardial ischemia on myocardial reparation in rats.Methods The myocardial ischemic injury models were established by hypodermic injection of high dose of ISO in rats.Surviving rats were randomly divided into experimental group and treated group,meanwhile control group was set.Then treated group was injected PDTC 100 mg/(kg·d)for 26 days.Myocardial pathomorphologic changes,NF-κBp65 activation,capillary density and myofibroblast accumulation were investigated.Then cardiac structure and function were assessed by echocardiography on day 14 and 28 of experiment.Results Cardiac necrotic areas were similar between experimental group and treated group.PDTC inhibited the activation of myocardial NF-κB,delayed the replacement of the damaged myocardium with granulation tissue,significantly depressed capillary density in the border area of necrosis and decreased myofibroblast accumulation in the zone of necrosis.The ratio of ventricular aneurysm formation in treated group was higher than experimental group.On day 28,the left ventricular functions in treated group were worse than that in experimental group.Conclusion Inhibition of NF-κB in the early phase after experimental myocardial ischemic injury in rats may be adverse to myocardial reparation,and may aggravate heart failure.

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潘波,杨成明,曾春雨,熊秀勤,王旭开,王红勇.大鼠缺血性心肌损伤后早期抑制核因子κB对心肌修复的影响[J].中国动脉硬化杂志,2009,17(4):281~284.

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  • 收稿日期:2009-02-17
  • 最后修改日期:2009-03-25
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