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首页> 外文期刊>Tropical Journal of Pharmaceutical Research >Effect of dexmedetomidine pretreatment on a rat model of myocardial ischemia-reperfusion injury
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Effect of dexmedetomidine pretreatment on a rat model of myocardial ischemia-reperfusion injury

机译:Dexmedetomidine预处理对心肌缺血再灌注损伤大鼠模型的影响

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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 ex pressions 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 ex pression 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.
机译:目的:研究Dexmedetomidine预处理对心肌缺血再灌注损伤的大鼠模型的影响(IRI)方法:使用三组SD大鼠(n = 48;平均体重= 275±25g)(每组16只大鼠) :假,IRI和Dexmedetomidine组。通过结扎左前冠状动脉建立缺血再灌注损伤(IRI)。用单一的I.P处理Dexmedetomidine基团的大鼠。在诱导IRI之前30分钟注射Dexmedetomidine(100μg/ kg)。通过酶联免疫吸附试验(ELISA)测定IL-1β,IL-6和TNF-α的血清水平。用于确定Bcl-2和Bax的蛋白质排版物的蛋白质印迹,而H&E染色测定大鼠心肌组织的组织病理学变化。结果:相对于假大鼠,IRI大鼠血清TNF-α,IL-1β和IL-6水平显着上调,但是通过Dexmedetomidine(P <0.05)降低。德克梅哌咪唑显着降低了IRI大鼠心肌组织中的丙二醛(MDA)的水平,但它增加了超氧化物歧化酶(SOD)活性(P <0.05)。它还显着增加了Bcl-2蛋白质水平,而蛋白质的蛋白质被降低(P <0.05)。 H&E染色的结果显示Dexmedetomidine显着缓解IRI诱导的损伤。结论:Dexmedetomidine通过抑制炎症和凋亡的变化,提高生理抗氧化潜力的大鼠心肌IRI。该发现可能对心肌缺血再灌注损伤的管理有用。

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