Protective effect of dexmedetomidine pre treatment against myocardial ischemia reperfusion injury in rats

• Published in: Tropical journal of pharmaceutical research Vol. 22; no. 2; pp. 349 - 354
• Main Authors: Sha, Qin, Jiang, Hui
• Format: Journal Article
• Language: English
• Published: 01.02.2023
• ISSN: 1596-5996; 1596-9827
• DOI: 10.4314/tjpr.v22i2.18

Purpose: To determine the protective effect of dexmedetomidine pre-treatment against myocardial ischemia-reperfusion injury (MRI), and the involvement of ER stress and protein kinase R-like ER enzyme (PERK) signaling pathway in the process. Methods: Sixty male Sprague-Dawley (SD) rats were assigned to three groups: sham, model (ischemia-reperfusion), and dexmedetomidine pre-treatment groups. Myocardial infarction area was measured using 2,3,5-triphenyl tetrazolium chloride (TTC) method. Changes in heart structure were examined using H & E, while myocardial cell apoptosis was determined with TUNEL assay. The protein expression levels of CHOP, glucose regulatory protein 78, ATF4, eukaryotic translation initiation factor 2-α (elf2-α), and PERK were assayed with Western blotting. Results: RPP, myocardial infarction area, myocardial cell apoptosis rate, and the expression levels of CHOP, GRP78, ATF4, elf2-α, and PERK were significantly raised, relative to sham. The structure of myocardial cells in sham-operated rats was intact and orderly. In contrast, the arrangement of myocardial cells in the model group was disordered, and the myofibrils were broken or wavy. However, the arrangement of myocardial cells in the dexmedetomidine group was significantly improved, when compared with the model group. Conclusion: Pretreatment with dexmedetomidine may exert a protective effect against MRI through suppression of ER stress and PERK signaling pathway. Further preclinical studies would be required to validate these findings.