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目的:分析腹主动脉缩窄诱导高血压大鼠心肌中肿瘤坏死因子-α(TNF-α)的合成,并探讨其调控机制。方法:选雄性SD大鼠,无菌条件下在腹主动脉放置银夹构建腹主动脉缩窄模型(腹主动脉缩窄组)。分别在术后1、3个月利用伊红-苏木精染色和磷钨酸苏木精染色评价左心室肥厚,免疫组化检测心肌中TNF-α含量,凝胶滞留实验筛选TNF-α可能的调控序列。结果:手术后3个月与假手术组大鼠相比,左心室出现显著肥厚,细胞面积分别为(429.4±57.6)μm2、(948.4±94.3)μm2,P<0.01。假手术组大鼠心肌TNFα-免疫组化染色为阴性,腹主动脉缩窄组手术后1、3个月大鼠心肌均显示强阳性。所有后负荷增加的心肌核蛋白与TNF-α上游序列的核转录因子(NF)-κB结合位点(-619~-591和-508~-481)的结合均高于后负荷正常的心肌。结论:左心室后负荷增加引起心肌TNF-α增高伴NF-κB核转移,TNF-α在心脏重构过程中起促进作用。
OBJECTIVE: To analyze the synthesis of tumor necrosis factor-α (TNF-α) in the myocardium of hypertensive rats induced by abdominal aorta constriction and to explore its regulatory mechanism. Methods: Male SD rats were selected and abdominal aorta constriction (abdominal aorta constriction group) was established by placing silver clip in abdominal aorta under aseptic conditions. Left ventricular hypertrophy was assessed by eosin-hematoxylin-eosin staining and phospho-tungstic acid hematoxylin staining at 1 and 3 months after operation, respectively. TNF-α levels in myocardium were detected by immunohistochemistry and TNF-α by gel retention assay Of regulatory sequences. Results: Compared with the sham operation group, left ventricular hypertrophy occurred at 3 months after operation. The area of the left ventricle was (429.4 ± 57.6) μm2 and (948.4 ± 94.3) μm2, respectively, P <0.01. In the sham operation group, the myocardial TNFα-immunohistochemical staining of the rats was negative. In the abdominal aorta constriction group, the myocardium of the rat myocardium showed strong positive one and three months after the operation. All post-load increased nuclear ribonucleoproteins were found to bind to NF-κB binding sites (-619 to -591 and -508 to -481) upstream of the TNF-α sequence more than normal post-load myocardium. Conclusion: The increase of left ventricular afterload induces the increase of myocardial TNF-α and NF-κB nuclear translocation, and TNF-α may play an important role in cardiac remodeling.