Open AccessEffect of dexmedetomidine pretreatment on a rat model of myocardial ischemia-reperfusion injury
Author(s) -
Jingxia Chen,
Wenyan Liu,
Shuzhen Wang,
Zidong Zhang,
Weiguo Li
Publication year - 2022
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v20i6.12
Subject(s) - dexmedetomidine , malondialdehyde , reperfusion injury , ischemia , medicine , superoxide dismutase , anesthesia , endocrinology , pharmacology , oxidative stress , sedation
Purpose: To study the effect of dexmedetomidine pretreatment on a rat model of myocardial ischemia-reperfusion injury (IRI)
Methods: Three groups of SD rats (n = 48; mean body weight = 275 ± 25 g) were used (16 rats each): sham, IRI, and dexmedetomidine groups. Ischemia-reperfusion injury (IRI) was established via ligation of left anterior coronary artery. Rats in dexmedetomidine group were treated with single i.p. injection of dexmedetomidine (100 μg/kg) 30 min before induction of IRI. Serum levels of IL-1β, IL-6 and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to determine the protein expressions of bcl-2 and bax, while histopathological changes in rat myocardial tissue were determined with H&E staining.
Results: Serum TNF-α, IL-1β and IL-6 levels were significantly up-regulated in IRI rats, relative to sham rats, but were decreased by dexmedetomidine (p < 0.05). Dexmedetomidine significantly reduced the level of malondialdehyde (MDA) in myocardial tissues of IRI rats, but it increased superoxide dismutase (SOD) activity (p < 0.05). It also markedly increased bcl-2 protein level, while the protein expression of bax was decreased (p < 0.05). Results of H & E staining showed that dexmedetomidine significantly mitigated IRI-induced damage.
Conclusion: Dexmedetomidine mitigates myocardial IRI in rats through suppression of inflammatory and apoptotic changes, and enhancement of physiological antioxidant potential. This finding may be useful for the management of myocardial ischemia-reperfusion injury.