摘要
Objective Ectoine is a natural compatible solute known for its cytoprotective properties, though its potential role in alleviatingdiabetic cardiomyopathy remains largely unexplored. This study aimed to examine the protective effects and underlying mechanismsof Ectoine on H9c2 cardiomyocytes under high-glucose and high-palmitic acid conditions. Methods The investigation included assessment of cell viability and lactate dehydrogenase release. Oxidative stress was evaluatedthrough measurements of reactive oxygen species, malondialdehyde levels, and superoxide dismutase activity. Inflammatory responseswere analyzed via TNF-α secretion and NF-κB and ERK1/2 pathways. Molecular docking studies were conducted to explore Ectoine-AMPK interaction, while mechanistic insightswere gained through examination of AMPK signaling, energy metabolism regulators, autophagic flux markers, and mitochondrialapoptosis. Results Ectoine treatment was associated with enhanced cell viability and reduced lactate dehydrogenase release. It appeared to alleviateoxidative stress through decreased reactive oxygen species and malondialdehyde levels, along with increased superoxide dismutaseactivity. Ectoine also showed suppressive effects on inflammatory responses, including reduced TNF-α secretion and inhibited NF-κB and ERK1/2 pathways. Molecular docking suggested binding affinity between Ectoine and AMPK (−6.4 kcal/mol). Mechanistically,Ectoine demonstrated potential in activating AMPK signaling, modulating energy metabolism, restoring autophagic flux, andattenuating mitochondrial apoptosis. Conclusion The findings suggest that Ectoine may protect against HG-PA-induced cardiomyocyte injury. This protective effect was associatedwith AMPK activation and the coordinated modulation of metabolic, autophagic, anti-inflammatory, and anti-apoptotic pathways.This study suggests the therapeutic potential of Ectoine and provides a basis for further investigation.
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