Key result
Salvia miltiorrhiza extract mitigates ischemic endothelial injury by regulating HIF-1α-mediated glycolysis and ferroptosis.
Salvia miltiorrhiza Bge. extract from above-ground parts ameliorates endothelial cell injury in myocardial infarction models by regulating HIF-1α mediated glycolysis and ferroptosis.
Salvia miltiorrhiza Bge. (S. miltiorrhiza) is an important herbal medicine, and the researches mainly focused on the roots of S. miltiorrhiza rather than the above-ground parts. Therefore, the detailed research on the above-ground parts of S. miltiorrhiza is still unclear. This study aimed to elucidate the constituents of the above-ground parts of S. miltiorrhiza extract (SME) and evaluate its effect on endothelial cell injury. For this purpose, the constituents of SME were identified by ultra performance liquid chromatography tandem mass spectrometry, and 41 compounds were determined, including terpenes, phenylpropanoids, flavonoids, sterols and phenolic acids. The effect of SME on endothelial cell was evaluated using isoproterenol (ISO)-treated C57BL/6 mice and hypoxia-treated HUVECs, and the results revealed that SME could improve endothelial cell injury in ISO-induced myocardial infarction model and hypoxia-induced HUVECs injury. In this process, SME could inhibit reactive oxygen species production, decrease the levels of malondialdehyde, lactic dehydrogenase, pyruvic acid, intracellular iron ions and sugar, and increase the levels of glutathione. Meanwhile, SME could improve the abnormal expressions of apoptosis-, glycolysis- and ferroptosis-related proteins. Taken together, our data demonstrated that SME treatment could alleviate endothelial cell injury by regulating HIF-1α mediated glycolysis and ferroptosis signals.
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Li et al. (2025) studied Endothelial cell injury and myocardial infarction. Salvia miltiorrhiza extract (SME) vs. Vehicle/Control was evaluated on Endothelial cell injury markers (ROS, MDA, LDH, pyruvic acid, iron ions, sugar, glutathione). Salvia miltiorrhiza extract treatment alleviated endothelial cell injury in ISO-induced myocardial infarction and hypoxia-induced HUVECs by regulating HIF-1α mediated glycolysis and ferroptosis.
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