右美托咪定抑制肾缺血/再灌注炎性反应

背景：在缺血/再灌注肾脏损伤的防治研究中，用药物激活或抑制机体某些因子从而保护肾组织，对肾移植和移植物的功能恢复有着重要意义。 目的：探索右美托咪定对大鼠肾缺血/再灌注炎性因子及C-X-C型趋化因子受体4表达的影响。 方法：40只大鼠随机等分为假手术组、缺血再灌注组、右美托咪定预处理组及右美托咪定后处理组。后3组行右肾切除，左肾缺血45 min，再灌注60 min，造肾缺血再灌注模型；右美托咪定预处理组于大鼠股静脉穿刺置管后泵注1 μg/kg右美托咪定，10 min后改为0.5 μg/kg，泵注30 min直至缺血即刻；右美托咪定后处理组于左肾再灌注后静脉泵注0.5 μg/kg右美托咪定 30 min。 结果与结论：肾脏缺血再灌注大鼠肾脏损伤严重，炎症明显，肾小管扩张，有肾小球肾炎表现，血清中白细胞介素1β和肿瘤坏死因子α水平显著升高(P < 0.05)，血清和肾脏中C-X-C型趋化因子受体4水平也明显增加(P < 0.05)；经右美托咪定预处理或后处理的肾缺血再灌注大鼠血清中白细胞介素1和肿瘤坏死因子α水平明显降低(P < 0.05)，血清和肾脏中C-X-C型趋化因子受体4水平也明显降低(P < 0.05)。提示肾缺血再灌注可致以炎性反应为特征的肾损伤；右美托咪定可以抑制炎性反应并弱化C-X-C型趋化因子受体4的表达，具有一定的肾保护作用。 中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程全文链接：

Dexmedetomidine inhibits renal ischemia/reperfusion-induced inflammatory reaction

BACKGROUND:Previous studies addressing the prevention and treatment of ischemia/reperfusion kidney damage show that, some drugs could activate or inhibit the body to protect kidney tissue, which is of great significance in renal transplantation and graft functional recovery. OBJECTIVE:To explore the influence of dexmedetomidine on expressions of inflammatory factors and C-X-C chemokine receptor type 4 in rat with renal ischemia/reperfusion. METHODS:Forty rats were randomly divided into four equal groups: sham group, ischemia/reperfusion group, dexmedetomidine preconditioning group and dexmedetomidine post-treatment group. Except the sham group, the right kidney was removed and the left kidney was subject to ischemia for 45 minutes and reperfusion for 60 minutes, thus establishing renal ischemia/reperfusion models in other three groups. As for preconditioning group, the rat femoral vein was punctured and transfused with 1 μg/kg dexmedetomidine for 10 minutes, followed by infusing 0.5 μg/kg dexmedetomidine for 30 minutes until ischemia occurred. As for posttreatment group, the rats were infused with 0.5 μg/kg dexmedetomidine for 30 minutes after reperfusion. RESULTS AND CONCLUSION: Serious kidney injury, obvious inflammation, tubular dilatation, and glomerulonephritis were found in rats with renal ischemia/reperfusion. The serum interleukin-1β and tumor necrosis factor-α levels in ischemia/reperfusion, dexmedetomidine preconditioning and dexmedetomidine post-treatment groups were increased significantly (P < 0.05). The expression of serum and renal C-X-C chemokine receptor type 4 was also increased (P < 0.05). Dexmedetomidine preconditioning or post-treatment significantly decreased serum interleukin-1β and tumor necrosis factor-α levels in rats with renal ischemia/reperfusion (P < 0.05). The same decline was observed in content of serum and renal C-X-C chemokine receptor type 4 (P < 0.05). Experimental findings indicate that renal ischemia/reperfusion can cause renal injury which is characterized by inflammatory reaction. Dexmedetomidine can reduce inflammatory reactions and attenuate C-X-C chemokine receptor type 4 expression to protect the kidney.