Dexmedetomidine attenuation of renal ischaemia-reperfusion injury requires sirtuin 3 activation
Dexmedetomidine attenuation of renal ischaemia-reperfusion injury requires sirtuin 3 activation
复制标题
右美托咪定减轻肾缺血再灌注损伤需要激活 Sirtuin 3
DOI：
10.1016/j.bja.2018.07.007
复制
发表时间：
2018-12-01
影响因子：
9.8
通讯作者：
Geng, Y.
中科院分区：
文献类型：
--
作者：
Si, Y.;Bao, H.;Geng, Y.
背景：右美托咪定可减轻肾缺血再灌注（I/R）损伤，但其作用机制尚不清楚。由于SIRT 3的激活可以减轻急性肾损伤，我们研究了右美托咪定是否通过SIRT 3减轻肾I/R损伤。方法：在缺氧/复氧的HK 2细胞和肾I/R的C57 BL/6 J小鼠中检测SIRT 3在右美托咪定减轻肾I/R损伤中的潜在参与。在一些实验中使用靶向SIRT 3的短干扰RNA来检查SIRT 3的潜在作用。在培养的细胞中分析细胞死亡和线粒体膜电位（Atm）。使用电子显微镜和肾功能标志物评估小鼠的线粒体损伤。结果：缺氧/复氧后HK 2细胞死亡率、细胞色素C表达、亲环素D乙酰化水平增加，Acl.ffn和SIRT 3表达降低（P
Background: Dexmedetomidine attenuates renal ischaemia and reperfusion (I/R) injury, but its mechanism of action is unclear. As sirtuin 3 (SIRT3) activation can alleviate acute kidney injury, we investigated whether dexmedetomidine acts through SIRT3 to reduce renal I/R injury.Methods: The potential involvement of SIRT3 in dexmedetomidine attenuation of renal I/R injury was tested in HK2 cells subjected to hypoxia/reoxygenation and C57BL/6J mice subjected to renal I/R. A short interfering RNA targeting SIRT3 was used in some experiments to examine the potential role of SIRT3. Cell death and mitochondrial membrane potential (Atm) were analysed in cultured cells. Mitochondrial damage in mice was assessed using electron microscopy and markers for renal function. Expression of cyclophilin D, cytochrome c, and SIRT3, and the level of cyclophilin D acetylation were determined.Results: Hypoxia/reoxygenation of HK2 cells increased cell death, cytochrome C expression, and cyclophilin D acetylation, and decreased Acl.ffn and SIRT3 expression (P