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本研究旨在探讨血管紧张素Ⅱ1型受体自身抗体(AT1-AA)在甲亢大鼠心肌肥大的表达及其与miRNA-350关系。将36只健康SD大鼠随机分为正常组及甲亢组,采用病理学、ELISA、RT-PCR和western blot等方法,比较甲亢组及对照组大鼠心肌肥大指标、AT1-AA、miRNA-350、AT1R mRNA及蛋白的表达;进一步将甲亢大鼠按AT1-AA检测结果分为AT1-AA阳性组和阴性组,比较两组miRNA-350、AT1R mRNA及蛋白的表达。结果显示,甲亢大鼠心肌肥大指标较正常大鼠均明显升高,且甲亢大鼠AT1-AA阳性率及A值明显高于对照组大鼠。甲亢组大鼠miRNA-350及AT1R的表达明显高于正常对照组,并深入研究发现AT1-AA阳性组miRNA-350及AT1R的表达亦高于AT1-AA阴性组。上述结论表明,AT1-AA参与甲亢大鼠心肌肥大的病理生理过程,miRNA-350在甲亢心肌肥大时AT1-AA的产生中发挥关键作用。
This study aimed to investigate the expression of angiotensin Ⅱ type 1 receptor autoantibodies (AT1-AA) in hypertrophic rats with cardiac hypertrophy and its relationship with miRNA-350. Thirty-six healthy SD rats were randomly divided into normal group and hyperthyroid group. Pathological, ELISA, RT-PCR and western blot methods were used to compare myocardial hypertrophy index, AT1-AA, miRNA-350 , AT1R mRNA and protein expression; further hyperthyroidism rats AT1-AA test results were divided into AT1-AA positive group and negative group, compared two groups of miRNA-350, AT1R mRNA and protein expression. The results showed that hyperthyroidism rat cardiac hypertrophy index were significantly higher than normal rats, and the positive rate of AT1-AA and A value of hyperthyroidism rats was significantly higher than that of the control group rats. The expression of miRNA-350 and AT1R in hyperthyroidism group was significantly higher than that in normal control group, and further study found that the expression of miRNA-350 and AT1R in AT1-AA positive group was also higher than that in AT1-AA negative group. These results indicate that AT1-AA is involved in the pathophysiological process of hypertrophy in hyperthyroid rats, and miRNA-350 plays a key role in the production of AT1-AA during hyperthyroid heart hypertrophy.