抗α1-肾上腺素受体抗体介导大鼠心室重塑的免疫机制

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目的观察抗α1肾上腺素受体自身抗体对大鼠心室重塑的影响并探索其可能机制。方法用α1肾上腺素受体胞外第二肽段合成肽免疫Wistar大鼠作为模型,设自发性高血压大鼠及正常Wistar大鼠为对照;用尾套法监测收缩压及心率,用酶联免疫吸附试验(ELISA)法检测抗α1肾上腺素受体抗体滴度,用光镜和电镜观察并计算心脏病理变化;用逆转录多聚合酶链式反应(RT PCR)、免疫印迹及免疫组织化学的方法检测左心室肌组织的c jun和/或c fos、α1肾上腺素受体的表达。结果在免疫后2周抗α1肾上腺素受体抗体滴度开始升高,并在整个实验过程中维持在较高水平;在实验过程中,免疫组血压心率与对照组差异无统计学意义,但均显著低于自发性高血压大鼠组;免疫组心脏体重比、左心室心肌细胞截面积、心肌胶原体积比例和心肌血管周围胶原面积与管腔面积比例分别为3.32mg/g±0.25mg/g、231μm2±11μm2、5.40%±0.66%和1.89±0.62,均显著高于正常对照组(分别为3.06mg/g±0.25mg/g、197μm2±19μm2、3.22%±0.15%和0.86±0.17),但低于自发性高血压大鼠组;电镜结果显示心肌细胞肥大、线粒体增多,心肌间质胶原纤维增多,说明免疫组发生心室重塑;在免疫组中,α1A、B肾上腺素受体及c fos的表达与正常对照差异无统计学意义,但α1D肾上腺素受体表? Objective To observe the effect of anti-α1 adrenergic receptor autoantibody on ventricular remodeling in rats and to explore its possible mechanism. Methods The Wistar rats were immunized with synthetic peptide of the second extracellular domain of α1 adrenoceptor. The spontaneous hypertensive rats and normal Wistar rats were used as controls. The systolic blood pressure and heart rate were monitored by the cuff method. Anti-α1 adrenergic receptor antibody titers were detected by ELISA. Cardiac pathological changes were observed by light microscopy and electron microscopy. Reverse transcription-polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry Methods The expression of c jun and / or c fos, α1 adrenoceptors in left ventricular muscle was detected. Results Anti-α1 adrenoceptor antibody titer began to increase 2 weeks after immunization and maintained at a high level throughout the experiment. During the experiment, there was no significant difference in blood pressure and heart rate between the two groups Were significantly lower than those in spontaneous hypertensive rats. The ratio of cardiac weight to weight, left ventricular myocardial cell cross-sectional area, ratio of myocardial collagen volume and perivascular collagen area to luminal area were 3.32mg / g ± 0.25mg / g, 231μm2 ± 11μm2, 5.40% ± 0.66% and 1.89 ± 0.62, respectively, were significantly higher than those of the normal control group (3.06mg / g ± 0.25mg / g, 197μm2 ± 19μm2, 3.22% ± 0.15% and 0.86 ± 0.17 respectively) , But lower than that of spontaneously hypertensive rats. Electron microscopy showed that cardiac myocytes hypertrophy, mitochondria increased and myocardial interstitial collagen fibers increased, indicating that the immune group had ventricular remodeling. In the immune group, α1A, B adrenergic receptor and The expression of c fos had no significant difference with the normal control, but α1D adrenoceptor table?
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