microRNA-23a在肝脏缺血再灌注损伤中的作用及机制研究

肝脏缺血再灌注损伤（HIRI）是外科实践中的一种常见的组织器官损伤，可使肝代谢解毒功能降低，微循环阻力升高，严重者还可导致肝功能衰竭，直接影响到疾病的预后、手术成功率和病人存活率，其发生机制及防治措施的研究现已成为外科领域的重点课题之一，但其具体机制迄今尚未完全阐明。近年来不断有研究证实，微小RNA（microRNA）在机体的各种生理病理过程中发挥着重要的调控作用。我们通过前期研究发现，MicroRNA-23a在HIRI病理过程中表达显著升高，缺血预处理干预后发生显著下调。本研究拟进一步证实MicroRNA-23a是否在HIRI中发挥加重损伤的调控作用以及可能的作用机制。本研究将首次从microRNA的角度对HIRI相关机制进行深入探讨，有望为今后的相关研究开阔新的思路。本研究结果也可能为HIRI的损伤评估提供新的检测指标，同时也可为HIRI的防治提供新的靶点和举措。

Hepatic ischemia-reperfusion (HIRI) is a common organic lesion during surgical practice, it can reduce the ability of hepatic metabolism and detoxication, increase the resistance of microcirculation,even lead to liver failure and influence the prognosis of hepatic surgery directly. Therefore, many efforts have been put into this area, but the precise mechanisms responsible for HIRI are still not well understood. In recent years,growing evidence demonstrates that microRNAs play important regulatory roles in many physiological processes. Our previous studies showed that the expression level of microRNA-23a was increased during HIRI, ischemic preconditioning could down-regulate such increase. Therefore,we suppose that the role of microRNA-23a is injurious in HIRI. This study intends to certify that microRNA-23a may aggravate the extent of HIRI，then investigate the molecular mechanisms behind this process.To the best of our knowledge, this study will be the first functional study to evaluate the role of microRNAs in liver ischemia injury.