Hyperthyroidism is known to increase the risk of ischemic heart diseases. Octreotide has been reported to attenuate ischemia/reperfusion (I/R) injury. Whether it is useful when ischemic heart disease is accompanied with co-morbidities like hyperthyroidism needs more clarifying. So, this study aimed to explore the effect of octreotide on cardiac I/R injury in hyperthyroid rats and to clarify if Nrf2 activation is involved in this effect. Forty adult female Wistar rats were subdivided into control (euthyroid) (n = 10) and hyperthyroid (n = 30) groups. Rats in hyperthyroid group received l-thyroxine (12 mg/L) in drinking water for 35 days, then were randomly divided into three equal subgroups (n = 10): hyperthyroid control positive group, hyperthyroid octreotide treated group, and hyperthyroid octreotide + Nrf2 inhibitor (brusatol) treated group. Isolated hearts were submitted to I/R and evaluated for cardiac hemodynamics and infarct size. Serum T3 and T4, coronary efflux lactate dehydrogenase (LDH) and creatine kinase-myoglobin binding (CK-MB) and cardiac tissue malondialdehyde (MDA) were estimated. Nrf2- regulated gene expressions of HO-1, SOD, GPx, and catalase were assessed. Octreotide administration to hyperthyroid rats improved baseline and post-ischemic recovery of cardiac hemodynamics, decreased the high coronary efflux LDH and CK-MB and tissue MDA, reduced infarction size, and upregulated the decreased antioxidative enzymes HO-1, SOD, GPx, and catalase mRNA expressions in the hyperthyroid I/R rat hearts. The Nrf2 inhibitor brusatol reversed the cardioprotective effect of octreotide in hyperthyroid I/R rat hearts. Octreotide can reduce oxidative stress to effectively alleviate I/R injury in the hyperthyroid rat hearts through upregulation of Nrf2-dependent antioxidative signaling pathways.

中文翻译：

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奥曲肽（生长抑素类似物）通过激活甲状腺功能亢进症大鼠模型中的核因子（类胡萝卜素衍生的2）样2（Nrf2）信号传导途径减轻心脏缺血/再灌注损伤

甲状腺功能亢进症会增加缺血性心脏病的风险。据报道，奥曲肽可减轻缺血/再灌注（I / R）损伤。当缺血性心脏病伴有甲状腺功能亢进等合并症时是否有用还需要进一步阐明。因此，本研究旨在探讨奥曲肽对甲状腺功能亢进大鼠心脏I / R损伤的影响，并阐明Nrf2激活是否与这种作用有关。将40只成年雌性Wistar大鼠分为对照组（正常甲状腺）（n = 10）和甲状腺功能亢进（n = 30）组。甲状腺功能亢进组的大鼠在饮用水中接受l-甲状腺素（12 mg / L），持续35天，然后随机分为三个相等的亚组（n = 10）：甲状腺功能亢进对照阳性组，甲状腺功能亢进奥曲肽治疗组和甲状腺功能亢进奥曲肽+ Nrf2抑制剂（brusatol）治疗组。离体心脏接受I / R治疗，并评估心脏血流动力学和梗死面积。估计血清T3和T4，冠状动脉外排乳酸脱氢酶（LDH）和肌酸激酶-肌红蛋白结合（CK-MB）和心脏组织丙二醛（MDA）。评估了HO-1，SOD，GPx和过氧化氢酶的Nrf2调控基因表达。给甲亢大鼠服用奥曲肽可改善基线和缺血后心脏血液动力学的恢复，降低冠状动脉外排LDH和CK-MB及组织MDA的含量，减少梗塞面积，并上调抗氧化酶HO-1，SOD，GPx和过氧化氢酶的减少甲亢I / R大鼠心脏中的mRNA表达。Nrf2抑制剂Brusatol逆转了奥曲肽对甲亢I / R大鼠心脏的心脏保护作用。