The insulin-like growth factor II receptor (IGF-IIR) induces myocardial hypertrophy under various pathological conditions like diabetes and hypertension via G protein receptors like Gαq or Gαs. Increased expression of the ligand IGF II and IGF-IIR induces pathological hypertrophy through downstream signaling mediators such as calcineurin, nuclear factor of activated T cells 3 and calcium-calmodulin (CaM)-dependent kinase II (CaMKII)-histone deacetylase 4 (HDAC4). The dried stigma of Crocus sativus L. (saffron) has a long repute as a traditional medicine against various disorders. In the present study, we have investigated whether C. sativus extract (CSE) canameliorate Leu²⁷IGF-II triggered hypertrophy and have elucidated the underlying mechanism of protection. Additionally, the effects of oleic acid (OA), an activator of calcineurin and CaMKII was investigated thereof. The results demonstrate that CSE can ameliorate Leu²⁷IGF-II-induced hypertrophy seemingly through regulation of calcineurin-NFAT3 and CaMKII-HDAC4 signaling cascade.

中文翻译：

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Leu27IGF-II 诱导的 H9c2 心肌细胞肥大被藏红花通过调节钙调神经磷酸酶/NFAT 和 CaMKIIδ 信号传导改善

胰岛素样生长因子 II 受体 (IGF-IIR) 通过 G 蛋白受体如 Gαq 或 Gαs 在糖尿病和高血压等各种病理条件下诱导心肌肥大。配体 IGF II 和 IGF-IIR 的表达增加通过下游信号传导介质诱导病理性肥大，如钙调神经磷酸酶、活化 T 细胞的核因子 3 和钙钙调蛋白 (CaM) 依赖性激酶 II (CaMKII)-组蛋白脱乙酰酶 4 (HDAC4) . Crocus sativus L.（藏红花）的干燥柱头作为治疗各种疾病的传统药物而享有盛誉。在本研究中，我们研究了苜蓿提取物 (CSE) 是否能改善 Leu ²⁷IGF-II 引发肥大并阐明了潜在的保护机制。此外，研究了其作为钙调神经磷酸酶和CaMKII的活化剂油酸(OA)的作用。结果表明，CSE似乎可以通过调节钙调神经磷酸酶-NFAT3 和 CaMKII-HDAC4 信号级联来改善 Leu ²⁷ IGF-II 诱导的肥大。