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The protective effect of ischemic preconditioning against hepatic ischemic-reperfusion injury under isoflurane anesthesia in rats

机译:缺血预处理对异氟烷麻醉下大鼠肝脏缺血再灌注损伤的保护作用

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Purpose: Apoptosis is a central mechanism of ischemic-reperfusion injury (IRI) to the liver. Among the methods to reduce IRI, ischemic preconditioning (IP) has been shown to confer protection. Therefore, the aim of this study was to determine if IP conferred protection against hepatic IRI under isoflurane anesthesia in rats and to investigate underlying protective mechanisms. Materials and Methods: Twenty-three rats weighing 270 to 300 grams were randomly divided into three groups: (1) the sham operated group (n = 5); (2) the non-IP group (n = 9; 45 minutes of hepatic ischemia followed by 2 hours of reperfusion); and (3) the IP group (n = 9); IP induced by 10 minutes of hepatic ischemia followed by 15 minutes of reperfusion before 45 minutes of prolonged hepatic ischemia). Anesthesia was maintained with isoflurane (1.5%). We compared the degrees of hepatic injury and expressions of B cell lymphoma 2 (Bcl-2) and caspase 3 and 8 mRNAs. Results: The IP group showed significantly lower levels of aspartate transaminase and alanine transaminase as well as reduced histological grades of hepatocyte injury compared with the non-IP group at 2 hours after reperfusion. At the corresponding time, the Bcl-2 mRNA level was 2-fold higher in the IP group. Caspase 3 mRNA levels were highest in the non-IP group significantly compared with the sham cohort. Similarly, caspase 8 mRNA levels were highest in the Non-IP group albeit not significancely. Conclusion: IP protected against hepatic IRI under isoflurane anesthesia in rats. The mechanism of protection appeared to involve upregulation of Bcl-2 expression resulting in inhibited apoptosis.
机译:目的:细胞凋亡是肝脏缺血再灌注损伤(IRI)的主要机制。在减少IRI的方法中,缺血预处理(IP)已被证明具有保护作用。因此,本研究的目的是确定IP是否在大鼠异氟烷麻醉下赋予了针对肝IRI的保护作用,并研究了潜在的保护机制。材料与方法:23只体重为270至300克的大鼠随机分为三组:(1)假手术组(n = 5); (2)非IP组(n = 9;肝缺血45分钟,再灌注2小时); (3)IP组(n = 9); IP由10分钟的肝缺血诱导,然后再进行15分钟的再灌注,然后延长45分钟的肝缺血。用异氟烷(1.5%)维持麻醉。我们比较了肝损伤的程度以及B细胞淋巴瘤2(Bcl-2)和caspase 3和8 mRNA的表达。结果:与非IP组相比,IP组在再灌注2小时后显示出明显降低的天冬氨酸转氨酶和丙氨酸转氨酶水平,并且降低了肝细胞损伤的组织学等级。在相应的时间,IP组的Bcl-2 mRNA水平高2倍。与假手术组相比,非IP组的Caspase 3 mRNA水平最高。同样,caspase 8 mRNA水平在非IP组中最高,尽管不显着。结论:IP在异氟烷麻醉下具有抗肝IRI的作用。保护的机制似乎涉及Bcl-2表达的上调,导致凋亡受到抑制。

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