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首页> 美国卫生研究院文献>Journal of Cellular and Molecular Medicine >Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin-interacting protein
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Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin-interacting protein

机译：急性高血糖会增强氧化应激并加重心肌缺血/再灌注损伤：硫氧还蛋白相互作用蛋白的作用

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Hyperglycaemia during acute myocardial infarction is common and associated with increased mortality. Thioredoxin-interacting protein (Txnip) is a modulator of cellular redox state and contributes to cell apoptosis. This study aimed to investigate whether or not hyperglycaemia enhances Txnip expression in myocardial ischaemia/reperfusion (MI/R) and consequently exacerbates MI/R injury. Rats were subjected to 30 min. of left coronary artery ligation followed by 4 hrs of reperfusion and treated with saline or high glucose (HG, 500 g/l, 4 ml/kg/h intravenously). In vitro study was performed on cultured rat cardiomyocytes subjected to simulated ischaemia/reperfusion (SI/R) and incubated with HG (25 mM) or normal glucose (5.6 mM) medium. In vivo HG infusion during MI/R significantly impaired cardiac function, aggravated myocardial injury and increased cardiac oxidative stress. Meanwhile, Txnip expression was enhanced whereas thioredoxin activity was inhibited following HG treatment in ischaemia/reperfusion (I/R) hearts. In addition, HG activated p38 MAPK and inhibited Akt in I/R hearts. In cultured cardiomyocytes subjected to SI/R, HG incubation stimulated Txnip expression and reduced thioredoxin activity. Overexpression of Txnip enhanced HG-induced superoxide generation and aggravated cardiomyocyte apoptosis, whereas Txnip RNAi significantly blunted the deleterious effects of HG. Moreover, inhibition of p38 MAPK or activation of Akt markedly blocked HG-induced Txnip expression in I/R cardiomyocytes. Most importantly, intramyocardial injection of Txnip siRNA markedly decreased Txnip expression and alleviated MI/R injury in HG-treated rats. Hyperglycaemia enhances myocardial Txnip expression, possibly through reciprocally modulating p38 MAPK and Akt activation, leading to aggravated oxidative stress and subsequently, amplification of cardiac injury following MI/R.
机译：急性心肌梗死中的高血糖很常见，并且与死亡率增加有关。硫氧还蛋白相互作用蛋白（Txnip）是细胞氧化还原状态的调节剂，有助于细胞凋亡。这项研究旨在调查高血糖症是否能增强心肌缺血/再灌注（MI / R）中的Txnip表达，从而加剧MI / R损伤。大鼠经受30分钟。左冠状动脉结扎术，然后再灌注4小时，并用盐水或高葡萄糖（HG，500 g / l，4 ml / kg / h静脉注射）治疗。对体外培养的大鼠心肌细胞进行了体外缺血/再灌注（SI / R），并与HG（25 mM）或正常葡萄糖（5.6 mM）孵育，进行了体外研究。 MI / R期间体内HG输注显着损害心脏功能，加重心肌损伤和增加心脏氧化应激。同时，缺血/再灌注（I / R）心脏中的HG处理后，Txnip表达增强，而硫氧还蛋白活性受到抑制。此外，HG激活了I / R心脏中的p38 MAPK并抑制了Akt。在经历SI / R的培养心肌细胞中，HG温育刺激了Txnip表达并降低了硫氧还蛋白的活性。 Txnip的过表达增强了HG诱导的超氧化物生成并加剧了心肌细胞的凋亡，而Txnip RNAi显着减弱了HG的有害作用。此外，p38 MAPK的抑制或Akt的激活明显阻断了I / R心肌细胞中HG诱导的Txnip表达。最重要的是，心肌内注射Txnip siRNA可以显着降低HG治疗大鼠的Txnip表达并减轻MI / R损伤。高血糖症可能通过相互调节p38 MAPK和Akt活化来增强心肌Txnip的表达，从而导致氧化应激加剧，继而导致MI / R后心脏损伤的扩大。

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