AI Article Synopsis
- The study examines how Esketamine (ESK) affects heart cell damage caused by lack of oxygen and subsequent reoxygenation, focusing on its interaction with TRPV1 and intracellular calcium levels.
- ESK treatment improved cell viability and reduced apoptosis and calcium concentration after H/R stress, highlighting its protective effects.
- The research suggests that while TRPV1 upregulation can diminish ESK's protective benefits, downregulating TRPV1 enhances its therapeutic impact against cardiac injury.
Article Abstract
Objective: This study aimed to investigate the effect of Esketamine (ESK) on the Hypoxia/Reoxygenation (H/R) injury of cardiomyocytes by regulating TRPV1 and inhibiting the concentration of intracellular Ca.
Methods: The H/R injury model of H9c2 cardiomyocytes was established after 4h hypoxia and 6h reoxygenation. H9c2 cells were treated with different concentrations of ESK or TRPV1 agonist capsaicin (10 μM) or TRPV1 inhibitor capsazepine (1 μM). Cell viability was detected by CCK-8 method, and apoptosis by flow cytometry. Intracellular Ca concentration was evaluated by Fluo-4 AM. LDH, MDA, SOD, and GSH-Px were detected with corresponding commercial kits. TRPV1 and p-TRPV1 proteins were detected by Western blot.
Results: After H/R, H9c2 cell viability decreased, apoptosis increased, intracellular Ca concentration increased, LDH and MDA levels increased, SOD and GSH-Px levels decreased, and p-TRPV1 expression increased. ESK treatment rescued these changes induced by H/R. After up-regulating TRPV1, the protective effect of ESK on H/R injury of H9c2 cells was weakened, while down-regulating TRPV1 could further protect against H/R injury.
Conclusion: ESK alleviates H/R injury of cardiomyocytes by regulating TRPV1 expression and inhibiting intracellular Ca concentration.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11070684 | PMC |
| http://dx.doi.org/10.1016/j.clinsp.2024.100363 | DOI Listing |
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