Ethnopharmacological relevance

Sympathetic hyperactivation is a significant risk factor in the development of cardiovascular disease. Safranal has shown good myocardial protection in recent studies, but the mechanism of its role in myocardial injury caused by sympathetic hyperactivation remains unclear.

Aim of the study

The purpose of this study was to investigate whether safranal can effectively reduce isoproterenol (ISO)-induced myocardial injury in rats and H9c2 cells and to reveal its pharmacological action and target in inhibiting myocardial injury caused by sympathetic hyperactivation.

Materials and methods

This study was carried out using network pharmacology, molecular docking, and in vitro and in vivo experiments. An in vivo model of myocardial injury was established by subcutaneous injection of ISO, and an in vitro model of H9c2 cell injury was induced by ISO.

Results

Safranal ameliorated myocardial injury caused by sympathetic hyperactivation by reducing the level of myocardial apoptosis. According to the results of network pharmacological analysis and molecular docking, the mechanism by which safranal alleviates myocardial injury may be closely related to the TNF signaling pathway, and safranal plays a role by regulating the core targets of the TNF signaling pathway. Safranal significantly inhibited the protein expression of TNF, PTGS2, MMP9 and pRELA.

Conclusion

Safranal plays a protective role in myocardial injury induced by sympathetic hyperactivation by downregulating the TNF signaling pathway.

中文翻译：

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基于网络药理学的番红花醛对异源性心肌损伤的作用及机制

民族药理学相关性

交感神经过度激活是心血管疾病发展的重要危险因素。番红花醛在近期研究中显示出良好的心肌保护作用，但其在交感神经过度激活引起的心肌损伤中的作用机制尚不清楚。

研究目的

本研究旨在探讨番红花醛能否有效减轻异丙肾上腺素（ISO）诱导的大鼠及H9c2细胞心肌损伤，揭示其抑制交感神经过度激活所致心肌损伤的药理作用及靶点。

材料和方法

本研究采用网络药理学、分子对接以及体外和体内实验进行。皮下注射ISO建立体内心肌损伤模型，体外诱导H9c2细胞损伤模型。

结果

番红花醛通过降低心肌细胞凋亡水平来改善交感神经过度激活引起的心肌损伤。网络药理学分析和分子对接结果表明，藏红花醛减轻心肌损伤的机制可能与TNF信号通路密切相关，藏红花醛通过调节TNF信号通路的核心靶点发挥作用。Safranal 显着抑制 TNF、PTGS2、MMP9 和 pRELA 的蛋白表达。

结论

Safranal 通过下调 TNF 信号通路对交感神经过度激活引起的心肌损伤起到保护作用。