Clemastine Fumarate alleviates endoplasmic reticulum stress through Nur77/GFPT2/CHOP pathway in the rat hearts after ischemia/reperfusion

Background: and Purpose Research shows that endoplasmic reticulum stress significantly influences cardiac cell death during myocardial ischemia-reperfusion (I/R) injury and that Clemastine Fumarate (CLE) can reduce this damage. This study used both in vivo and in vitro tests to confirm how CLE works. Experimental Approach We developed a rat model of cardiomyocyte hypoxia/reoxygenation (H/R) and a rat model of myocardial ischemia/reperfusion (I/R) injury. These models were used to evaluate cardiac function, myocardial infarction size, and tissue morphology. We also analyzed rat serum for inflammatory agents and cardiac damage indicators, including the expression levels of Nur77, GFPT2, and CHOP. These findings aimed to investigate the mechanism of CLE. All experimental data were expressed as the mean ± standard deviation (SD). One-way ANOVA was used to compare multiple groups, and the significance of differences among outcomes in inter-group pairwise comparisons was assessed using the Student-Newman-Keuls technique. A value of p< 0.05 was considered statistically significant. Key Results Our study showed that CLE can alleviate myocardial I/R injury and ER stress via the Nur77/GFPT2/CHOP signaling pathway. This finding offers theoretical support for both preventing and treating perioperative myocardial I/R injury. Additionally, it highlights the potential application of CLE in perioperative care. Conclusion and Implications Our study showed that CLE can alleviate myocardial I/R injury and ER stress via the Nur77/GFPT2/CHOP signaling pathway. This finding offers theoretical support for both preventing and treating perioperative myocardial I/R injury. Additionally, it highlights the potential application of CLE in perioperative care.