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目的观察甲亢心肌肥大大鼠血清血管紧张素Ⅱ1型受体自身抗体(AT1-AA)与心肌组织磷脂酰肌醇-3-激酶(PI3K)、蛋白激酶B(Akt)的表达,探讨AT1-AA在甲亢大鼠心肌肥大中的作用及其与PI3K/Akt信号通路的关系。方法将54只SD大鼠随机分为3组:甲亢组、甲亢+奥美沙坦组及对照组,每组18只,前2组灌服左甲状腺素钠制备甲亢大鼠模型,甲亢+奥美沙坦组同时给予奥美沙坦。以心脏质量指数(HWI)和心钠肽(ANP)mRNA作为心肌肥大指标,采用酶联免疫吸附法(ELISA)检测大鼠血清AT1-AA,并通过蛋白质印迹法检测各组大鼠血管紧张素Ⅱ1型受体(AT1R)和PI3K/p-Akt的表达水平;根据AT1-AA检测结果,将甲亢组和甲亢+奥美沙坦组大鼠分为AT1-AA阳性组和阴性组,比较AT1-AA阳性组和阴性组AT1R及PI3K/p-Akt的表达情况。结果 (1)与对照组比较,甲亢组、甲亢+奥美沙坦组大鼠HWI增加,ANP mRNA相对表达量升高(P均<0.05);甲亢组大鼠HWI及ANP mRNA相对表达量亦高于甲亢+奥美沙坦组大鼠(P<0.05)。(2)甲亢组、甲亢+奥美沙坦组大鼠AT1-AA阳性率及光密度(D)值(61.11%,72.22%和0.44±0.12,0.49±0.08)高于对照组(16.67%和0.28±0.05,P均<0.01)。(3)甲亢组、甲亢+奥美沙坦组大鼠AT1R和PI3K/pAkt的表达较对照组升高(P<0.05,P<0.01);与甲亢组相比,甲亢+奥美沙坦组大鼠心肌组织PI3K、p-Akt表达水平均降低(P<0.01,P<0.05)。(4)甲亢组大鼠中,AT1-AA阳性组PI3K/p-Akt的表达明显高于AT1-AA阴性组(P<0.01);甲亢+奥美沙坦组大鼠中,AT1-AA阳性组PI3K/p-Akt的表达较AT1-AA阴性组降低(P<0.05)。结论 AT1-AA可能通过AT1R激活PI3K/Akt信号通路参与甲亢心肌肥大病理生理过程。
Objective To investigate the expression of AT1-AA and PI3K, Akt in hypertrophic rats with hypertrophic heart hypertrophy, and to explore the role of AT1-AA The Role of PI3K / Akt Signal Pathway in Hyperthyroidism Induced Myocardial Hypertrophy in Rats. Methods 54 Sprague-Dawley rats were randomly divided into three groups: hyperthyroidism group, hyperthyroidism + olmesartan group and control group, with 18 rats in each group. The first two groups were given hyperthyroidism by levothyroxine sodium, hyperthyroidism + Tan group also given olmesartan. The heart weight index (HWI) and atrial natriuretic peptide (ANP) mRNA were used as indexes of cardiac hypertrophy. Serum AT1-AA was detected by enzyme-linked immunosorbent assay (ELISA), and angiotensin The expression of AT1R and PI3K / p-Akt in AT1-AA group and AT1-AA positive group were detected by AT1-AA test. AA positive group and negative group AT1R and PI3K / p-Akt expression. Results (1) Compared with the control group, the HWI and the relative expression of ANP mRNA in hyperthyroidism and hyperthyroidism + olmesartan groups were increased (all P <0.05); the relative expression of HWI and ANP mRNA in hyperthyroidism group was also high Hyperthyroidism + olmesartan group rats (P <0.05). (2) The positive rate and optical density (AT) of AT1-AA in hyperthyroidism group and hyperthyroidism + olmesartan group were significantly higher than those in the control group (61.11%, 72.22% and 0.44 ± 0.12,0.49 ± 0.08) ± 0.05, P <0.01). (3) The expression of AT1R and PI3K / pAkt in hyperthyroidism group and hyperthyroidism + olmesartan group was higher than that in control group (P <0.05, P <0.01). Compared with hyperthyroidism group, the expression of AT1R and PI3K / Myocardial PI3K, p-Akt expression levels were reduced (P <0.01, P <0.05). (4) The expression of PI3K / p-Akt in AT1-AA positive group was significantly higher than that in AT1-AA negative group in hyperthyroidism group (P <0.01); in AT1-AA positive group The expression of PI3K / p-Akt was lower than that of AT1-AA negative group (P <0.05). Conclusion AT1-AA may be involved in the pathophysiological process of hypertrophic cardiomyopathy by the activation of PI3K / Akt signaling pathway by AT1R.