Protective effects of Dex on myocardial injury induced by hepatic cold ischemia reperfusion

Hongxia Li, Y. Weng, Wenli Yu
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Abstract

Objective To explore the effects of dexmedetomidine on myocardial injury during liver cold ischemia reperfusion in rats. Methods A total of 40 healthy male Sprague-Dawley (SD)rats with a weight of 220~250 gram and an age of 8~10 weeks were randomly divided into 5 groups of sham, model, Dex, Atip and AG490 by a random number table (n=8 each). At 8h post-reperfusion, blood samples were harvested from infra-hepatic vena cava and serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), creatine kinase-muscle/brain (CK-MB), troponin I (cTnI)and heart-type fatty acid binding protein (H-FABP)determined by enzyme-linked immunosorbent assay (ELISA). After blood sampling, the rats were sacrificed, the expression of activated caspase-3 was detected by immunohistochemistry and apoptotic cells by TUNEL.Apoptotic rate was calculated.And the phosphorylations of JAK2, STAT1 and STAT3 were assessed by Western blot. Results As compared with sham group, the levels of TNF-α, IL-6, CK-MB, cTnI and H-FABP significantly increased, apoptotic rate spiked, pathological damage worsened and the expressions of activated caspase-3, p-JAK2, p-STAT1 and p-STAT3 were up-regulated in other groups (P<0.05); As compared with model group, the levels of TNF-α, IL-6, CK-MB, cTnI and H-FABP significantly decreased, apoptotic rate declined, pathological damage became alleviated and the expressions of activated caspase-3, p-JAK2, p-STAT1 and p-STAT3 became down-regulated in groups Dex and AG490 (P<0.05); as compared with group Dex, the levels of TNF-α, IL-6, CK-MB, cTnI and H-FABP significantly increased, apoptotic rate rose, pathological damage worsened and the expressions of activated caspase-3, p-JAK2, p-STAT1 and p-STAT3 became up-regulated in group Atip (P<0.05). Conclusions Dexmedetomidine can ameliorate myocardial injury induced by liver cold ischemia-reperfusion in rats. Key words: Liver; Reperfusion injury; Myocardium; Apoptosis
右美托咪唑对肝冷缺血再灌注心肌损伤的保护作用
目的探讨右美托咪定对大鼠肝脏冷缺血再灌注心肌损伤的影响。方法选取体重220~250 g、8~10周龄的健康雄性SD大鼠40只,采用随机数字表法随机分为假手术组、模型组、Dex组、Atip组和AG490组,每组8只。再灌注后8h取肝下腔静脉采血,采用酶联免疫吸附试验(ELISA)测定血清肿瘤坏死因子-α (TNF-α)、白细胞介素-6 (IL-6)、肌酸激酶-肌脑(CK-MB)、肌钙蛋白I (cTnI)和心型脂肪酸结合蛋白(H-FABP)水平。取血后处死大鼠,免疫组化检测活化caspase-3的表达,TUNEL检测凋亡细胞。计算细胞凋亡率。Western blot检测JAK2、STAT1、STAT3的磷酸化水平。结果与假手术组比较,其余各组细胞TNF-α、IL-6、CK-MB、cTnI、H-FABP水平均显著升高,细胞凋亡率升高,病理损伤加重,活化caspase-3、P - jak2、P - stat1、P - stat3表达上调(P<0.05);与模型组比较,Dex组和AG490组大鼠外周血中TNF-α、IL-6、CK-MB、cTnI、H-FABP水平显著降低,细胞凋亡率下降,病理损伤减轻,活化caspase-3、P - jak2、P - stat1、P - stat3表达下调(P<0.05);与Dex组比较,Atip组TNF-α、IL-6、CK-MB、cTnI、H-FABP水平显著升高,细胞凋亡率升高,病理损伤加重,活化caspase-3、P - jak2、P - stat1、P - stat3表达上调(P<0.05)。结论右美托咪定可改善大鼠肝脏冷缺血再灌注所致的心肌损伤。关键词:肝脏;再灌注损伤;心肌;细胞凋亡
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