Heart failure (HF) and cardiac hypertrophy is an unfavorable outcome of pathological cardiac remodeling and represents the most important contributing factor for HF and cardiac hypertrophy. Amygdalin (AMG) is a cyanogenic glycoside derived from bitter almonds. Accumulating evidences have highlighted their pharmacological potentials against various diseases. However, there is no report delineating the potential of AMG against angiotensin (Ang II) induced cardiac injuries. Thus, the present study was performed to explore whether AMG could ameliorate Ang II induced cardiomyopathies and thereby ascertain the underlying mechanisms thereof. To this end, H9c2 cells were treated with Ang II and thereafter treated with various concentration of AMG and finally the cardio-protective effects of AMG were analyzed through Western blotting, immunofluorescence, and insilico analysis. Our results showed that the cardiomyocyte cell size, inflammatory markers and cytokines(pNF-κB, TNF-α, iNOS and COX-2) were markedly increased following Ang II treatment; nevertheless, treatment with AMG led to considerable decrement in the Ang II induced enlargement of the cardiomyocytes, and attenuate the expression of hypertrophic markers(ANP, BNP and MHC-7), inflammatory markers and cytokines. Additionally, oxidative stress related proteins (Nrf2, catalase, SOD-2, and GPX-4) were markedly increased following AMG treatment. Molecular docking reveals the interaction of AMG with Nrf2 possessing good binding affinity. Cumulatively, our study highlights the cardio-protective role of AMG against Ang II induced cardiomyopathies, including oxidative stress and inflammation effects. The intriguing in vitro results warrants the need of further animal studies to truly ascertain their potentialities.

中文翻译：

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苦杏仁苷通过调节 Nrf2 和 NF-κB 活化对血管紧张素 II 诱导的心脏肥大、氧化应激和炎症反应的心脏保护作用

心力衰竭 (HF) 和心脏肥大是病理性心脏重塑的不利结果，是导致 HF 和心脏肥大的最重要因素。苦杏仁苷 (AMG) 是一种源自苦杏仁的氰苷。越来越多的证据突出了它们对各种疾病的药理潜力。然而，没有报告描述 AMG 对血管紧张素 (Ang II) 诱导的心脏损伤的潜力。因此，本研究旨在探索 AMG 是否可以改善 Ang II 诱导的心肌病，从而确定其潜在机制。为此，H9c2 细胞用 Ang II 处理，然后用不同浓度的 AMG 处理，最后通过蛋白质印迹、免疫荧光、和 insilico 分析。我们的研究结果表明，Ang II 治疗后心肌细胞大小、炎症标志物和细胞因子（pNF-κB、TNF-α、iNOS 和 COX-2）显着增加；然而，AMG 治疗导致 Ang II 诱导的心肌细胞增大显着减少，并减弱了肥大标志物（ANP、BNP 和 MHC-7）、炎症标志物和细胞因子的表达。此外，AMG 处理后，氧化应激相关蛋白（Nrf2、过氧化氢酶、SOD-2 和 GPX-4）显着增加。分子对接揭示了 AMG 与具有良好结合亲和力的 Nrf2 的相互作用。总的来说，我们的研究强调了 AMG 对 Ang II 诱导的心肌病的心脏保护作用，包括氧化应激和炎症作用。