Cytoskeleton-disrupting agent cytochalasin B reduces oxidative stress caused by high glucose in the human arterial smooth muscle
Cytoskeleton-disrupting agent cytochalasin B reduces oxidative stress caused by high glucose in the human arterial smooth muscle
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细胞骨架破坏剂细胞松弛素 B 可减少人动脉平滑肌中高葡萄糖引起的氧化应激
DOI：
10.1016/j.jphs.2020.08.004
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发表时间：
2020
影响因子：
3.5
通讯作者：
Kitahata Hiroshi
中科院分区：
文献类型：
--
作者：
Takaishi Kazumi;Kinoshita Hiroyuki;Feng Guo-Gang;Azma Toshiharu;Kawahito Shinji;Kitahata Hiroshi
细胞骨架动力学在氧化应激对人体血管系统的作用还不清楚。目前的研究检查了细胞分裂素破坏剂细胞松弛素B是否能减少人体动脉平滑肌中由高糖引起的氧化应激。所有实验均在无内皮的人网膜动脉或培养的人冠状动脉平滑肌细胞中进行，葡萄糖浓度为5.5mmol/L。20 mmol/L葡萄糖暴露60 min可使ATP敏感性K+通道（KATP）开放剂左旋克罗卡林（levcromakalim，10 - 8 ~ 3 × 10 - 6 mol/L和3 × 10 - 6 mol/L）引起的舒张或超极化减弱。细胞松弛素B和超氧化物抑制剂Tiron，恢复他们类似。细胞松弛素B降低NADPH氧化酶活性，导致高糖处理动脉的超氧化物水平降低。此外，细胞松弛素B损害了高糖处理的动脉平滑肌细胞中的F-肌动蛋白结构和NADPH氧化酶亚基p47 phox的膜转位。临床浓度的细胞松弛素B通过高糖引起的氧化应激预防人血管平滑肌功能障碍。细胞骨架的调节可能是维持高血糖患者正常血管功能所必需的。
The role of cytoskeleton dynamics in the oxidative stress toward human vasculature has been unclear. The current study examined whether the cytoskeleton-disrupting agent cytochalasin B reduces oxidative stress caused by high glucose in the human arterial smooth muscle. All experiments in the human omental arteries without endothelium or the cultured human coronary artery smooth muscle cells were performed ind-glucose (5.5 mmol/L). The exposure towardd-glucose (20 mmol/L) for 60 min reduced the relaxation or hyperpolarization to an ATP sensitive K+channel (KATP) opener levcromakalim (10−8to 3 × 10−6mol/L and 3 × 10−6mol/L, respectively). Cytochalasin B and a superoxide inhibitor Tiron, restored them similarly. Cytochalasin B reduced the NADPH oxidase activity, leading to a decrease in superoxide levels of the arteries treated with highd-glucose. Also, cytochalasin B impaired the F-actin constitution and the membrane translocation of an NADPH oxidase subunit p47phox in artery smooth muscle cells treated with highd-glucose. A clinical concentration of cytochalasin B prevented human vascular smooth muscle malfunction via the oxidative stress caused by high glucose. Regulation of the cytoskeleton may be essential to keep the normal vascular function in patients with hyperglycemia.