Basic & Clinical Medicine ›› 2026, Vol. 46 ›› Issue (4): 540-546.doi: 10.16352/j.issn.1001-6325.2026.04.0540

• Original Articles • Previous Articles     Next Articles

Cinnamic acid alleviates anoxia/reoxygenation-induced injury of rat myocardial cell line

HAN Liting1, WANG Yan2*, CHEN Xing1, MA Jia1, LIU Yang1   

  1. 1. Department of Cardiac Rehabilitation; 2. Department of Cardiology, Zhengzhou Seventh People′s Hospital, Zhengzhou 450008, China
  • Received:2025-05-09 Revised:2025-09-24 Published:2026-03-24
  • Contact: *15836089367@163.com

Abstract: Objective To explore the mechanism of cinnamic acid (CA) in improving anoxia/reoxygenation (A/R)-induced myocardial cell injury. Methods H9c2 cells were assigned into control group, A/R group, low-dose and high-dose groups of cinnamic acid, HIF-1α activator (DMOG) group, and high-dose cinnamic acid+HIF-1α inhibitor (IDF-11774) group. Cell viability was assessed using the CCK-8 assay. Levels of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) in the supernatant were measured by ELISA. Mitochondrial ultrastructure was observed via transmission electron microscopy. Intracellular reactive oxygen species (ROS) and ferrous iron (Fe2+) levels were detected using 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) and FerroOrange fluorescent probes, respectively. Malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were determined using commercial kits. Protein expression of HIF-1α, SLC7A11, and GPX4 was analyzed by Western blot. Results Compared with the control group, the A/R group exhibited mitochondrial atrophy, severe cristae disruption, and partial outer membrane rupture. Additionally, cell viability and SOD activity, along with HIF-1α, SLC7A11, and GPX4 protein levels, were significantly decreased, whereas LDH and CK-MB release, ROS production, MDA levels, and Fe2+ accumulation were significantly increased (P<0.05). Compared with the A/R group, the low and high-dose cinnamic acid groups, and DMOG group showed reduced mitochondrial structural injury in H9c2 cells, raised cell viability, SOD activity, HIF-1α, SLC7A11, and GPX4 proteins, and decreased cell supernatant LDH, CK-MB levels, cell ROS fluorescence intensity, MDA and Fe2+ fluorescence intensity (P<0.05). IDF-11774 attenuated the inhibitory effect of high-dose cinnamic acid on A/R induced ferroptosis in H9c2 cells and its improvement effect on cell injury. Conclusions Cinnamic acid alleviates A/R-induced cardiomyocyte injury by inhibiting ferroptosis, likely through activation of the HIF-1α/SLC7A11/GPX4 signaling pathway.

Key words: cinnamic acid, anoxia/reoxygenation, myocardial cells, ferroptosis

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