AT1受体肽诱发大鼠心肌免疫损伤的实验研究

Y Luo, Y Liao, M Wang, Y Wei, J Dong, I Wang, Y Lu
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摘要

为了研究用AT1受体肽免疫大鼠的免疫损伤,18只雄性Wistar大鼠分为两组:免疫组(n = 12),每只大鼠用150微克AT1受体肽偶联牛血清白蛋白和弗氏佐剂免疫。对照组(n = 6)为假免疫,"免疫液 "除AT1受体肽外与免疫组相同。采用尾袖带技术测量收缩压(SBP),用ELISA方法检测AT1受体肽抗体,用光镜和电子显微镜观察左心室心肌和肾皮质切片。免疫组与对照组的 SBP 和组织切片的光镜观察无明显差异。免疫组大鼠抗AT1受体肽抗血清的O.D.值明显高于免疫前大鼠和对照组(P < 0.01)。免疫组的阳性率为 100%,而对照组为 0%。超微形态学显示了潜在的心肌损伤,包括:线粒体数量增加,许多线粒体肿胀,嵴数量减少或缺失,嵴溶解,心肌纤维紊乱,心肌纤维破坏和心肌溶解。肾小管上皮细胞溶酶体增加。AT1受体肽可诱导产生抗AT1受体肽抗体,导致大鼠心肌和肾脏损伤。
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Experimental study on AT1-receptor-peptide-induced myocardial immune damage in rat.

In order to investigate the immunological damage in rat immunized with AT1-receptor peptide, 18 male Wistar rats were divided into two groups: immunized-group (n = 12), each rat was immunized with 150 micrograms AT1-receptor peptide coupled to bovine serum albumin, together with Freund's adjuvant. Control group (n = 6), sham-immunized, "immunized liquid" was same as immunized-group except AT1-receptor peptide. Systolic blood pressure (SBP) was measured by using the tail-cuff technique, antibody against AT1-receptor peptide detected by using ELISA method, and left ventricular myocardium and renal cortex sections were observed under light and electron microscopy. There was no significant difference in SBP and light microscopic observation of the tissue sections between the immunized-group and control group. The O.D. value of anti-AT1-receptor peptide antiserum was significantly higher in the immunized-group than in the rats before immunization and control group (P < 0.01). Positive rate in the immunized-group was 100%, while 0% in the control group. Ultramicroscopic morphology showed potential myocardial injury, including: increase in number of mitochondria, swelling of many mitochondria with reduction in number or absence of their cristae and cristolysis, disorder of the cardiac myofibrils, and myofibrillar disruption and myocytolysis. And lysosomes were increased in renal tubular epithelia. The AT1-receptor peptide could induce to generate the antibody against AT1-receptor peptide and lead to myocardial and renal damage in rats.

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