Dezocine Suppresses Myocardial Cell Apoptosis in Rats with Myocardial Ischemia-Reperfusion Injury via TLR4/NF-κB Signaling Pathway
Mingyan He1★, Ru Liu1, Yalin Li1, Qi Zhang2★ Corresponding author
- 1Department of Anesthesiology, Hunan Provincial People’s Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, Hunan, CHINA.
- 2Hunan Base, Engineering Technology Branch, China Southern Airlines Co., Ltd., Changsha, CHINA.
CORRESPONDENCE
Mingyan He
Department of Anesthesiology, Hunan Provincial People’s Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, Hunan, CHINA.
Received: 08-01-2025; Accepted: 14-02-2025.
Volume 22, Issue 1 · pp. 217–222 · PUBLISHED 2026 · DOI: 10.1177/09731296251325341
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ABSTRACT
Background: Myocardial ischemia-reperfusion (MI/R) injury is a leading cause of myocardial damage, characterized by apoptosis and impaired cardiac function. Dezocine, a mixed opioid receptor agonist/antagonist, has shown potential in mitigating MI/R injury, but its underlying mechanisms remain unclear. Objectives: This study aimed to evaluate the effects of dezocine on myocardial cell apoptosis in rats with MI/R injury, focusing on the TLR4/NF-κB signaling pathway. Materials and Methods: Thirty-six Sprague-Dawley rats were randomly divided into three groups: sham, model, and dezocine (n = 12 each). The sham group underwent thoracotomy without MI/R injury. The model group received normal saline prior to MI/R injury induction, while the dezocine group was administered dezocine. Toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) p65 expression were analyzed using immunohistochemistry. Western blotting quantified Bax and Caspase-3 protein levels while quantitative polymerase chain reaction assessed their mRNA expression. Cell apoptosis was evaluated via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Results: TLR4 and NF-κB p65 expression were significantly elevated in the model and dezocine groups compared to the sham group but notably lower in the dezocine group versus the model group. Bax and Caspase-3 protein and mRNA levels followed a similar trend. TUNEL assay results demonstrated higher apoptosis rates in the model and dezocine groups compared to the sham group, with the dezocine group showing a marked reduction in apoptosis compared to the model group (p < 0.05). Conclusion: Dezocine suppresses the TLR4/NF-κB pathway, reducing myocardial apoptosis in MI/R injury, suggesting its potential as a therapeutic agent in mitigating cardiac damage.
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He, M., Liu, R., Li, Y., & Zhang, Q. (2026). Dezocine Suppresses Myocardial Cell Apoptosis in Rats with Myocardial Ischemia-Reperfusion Injury via TLR4/NF-κB Signaling Pathway. Pharmacognosy Magazine, 22(1), 217–222. https://doi.org/10.1177/09731296251325341
