右美托咪定对肾缺血／再灌注损伤保护作用的研究现状

Protective effect of dexmedetomidine on renal ischemia/reperfusion injury

背景肾缺血／再灌注损伤（ischemia／reperfusion injury，I／RI）成为影响术后患者康复及生存率的重要因素。研究证实右美托咪定（dexmedetomidine，Dex）对肾I／RI有保护作用。目的综述Dex对肾I／RI的保护作用及机制的研究进展。内容Dex通过清除氧自由基、抗氧化作用、减轻氧化应激反应造成的损伤、抗炎作用、抗凋亡作用、改善线粒体功能以及抑制ianus激酶2，信号转导因子和转录活化因子3（ianus kinase 2／signal transducer and activator of transcription3，JAK2／STAT3）、Toll样受体4（Toll-like receptors4，TLR4）信号转导通路和激活磷酸肌醇3激酶／蛋白激酶B（phosphatidylinositide 3 kinase／protein kinaseB，H3K／Akt）、沉默信息调节因子2相关酶3（silent information regulator 2 homolog3，SIRT3）信号转导通路对肾I／RI发挥保护作用。趋向Dex对肾I／RI的保护作用及其机制目前仍在研究中，有望在更深入理解的基础上为临床治疗措施提供有力证据。

Background Renal ischemia/reperfusion injury （I/RI） is one of the most important postoperative complications affecting the recovery and survival of patients. It has been shown that dexmedetomidine （Dex） mitigates renal I/RI. Objective To review the potential mechanisms underlying the protective effect of Dex on renal I/RI. Content Accumulating evidence shows that Dex may protect the kidney through controlling several cellular events and regulating multiple signal transduction pathways, which are mobilized in renal I/RI. In addition to its antioxidant property to scavenge oxygen free radical and reduce oxidative stress, Dex can also inhibit inflammation and apoptosis, and improve mitoehondrial function. The potential signal transduetion pathways involved in the benefits of Dex to renal I/RI include janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3）, Toll-like receptors 4 （TLR4）, phosphatidylinositide 3 kinase/protein kinase B （PI3K/Akt）, and silent information regulator 2 homolog 3 （SIRT3）, etc. Trend Further investigations should be conducted to elucidate the potential targets of Dex, which are able to be transformed for clinical intervention and treatment of renal I/RI.