Sun Li-na, Li Liao-liao, Li Zheng-bin, Wang Ling, Wang Xiao-liang
Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Acta Pharmacol Sin. 2008 Oct;29(10):1150-6. doi: 10.1111/j.1745-7254.2008.00853.x.
TREK-1 (TWIK-related K+ channel-1) is a 2-pore-domain K+ channel subtype. The present study investigated the role of TREK-1 in cell death induced by oxidative stress.
The cell viability of wild-type Chinese hamster ovary (CHO) and TREK-1-transfected CHO cells (TREK-1/CHO cells) was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in the presence of sodium nitroprusside (SNP) or hydrogen peroxide (H2O2). Apoptosis of wild-type CHO and TREK-1/CHO cells was detected using Hoechst33342 staining.
Both SNP and H2O2 caused dose- and time-dependent growth inhibition of wild-type CHO and TREK-1/ CHO cells. Following a 12 h exposure to SNP, the 50% inhibition (IC(50)) values for wild-type CHO and TREK-1/CHO cells were calculated as 0.69 mmol/L and 1.14 mmol/L, respectively. The IC(50) values were 0.07 mmol/L and 0.09 mmol/L in H2O2-treated wild-type CHO and TREK-1/CHO cells, respectively, following 12 h exposure to H2O2. Moreover, SNP/H2O2 induced less apoptosis in TREK-1/ CHO cells than that in wild-type CHO cells (P<0.05).
The results demonstrated that TREK-1 played a protective role against oxidative injury.
TREK-1（TWIK相关钾离子通道-1）是一种双孔结构域钾离子通道亚型。本研究旨在探讨TREK-1在氧化应激诱导的细胞死亡中的作用。
在硝普钠（SNP）或过氧化氢（H2O2）存在的情况下，使用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐（MTT）法检测野生型中国仓鼠卵巢（CHO）细胞和转染了TREK-1的CHO细胞（TREK-1/CHO细胞）的细胞活力。使用Hoechst33342染色检测野生型CHO细胞和TREK-1/CHO细胞的凋亡情况。
SNP和H2O2均导致野生型CHO细胞和TREK-1/CHO细胞出现剂量和时间依赖性的生长抑制。在暴露于SNP 12小时后，野生型CHO细胞和TREK-1/CHO细胞的50%抑制（IC(50)）值分别计算为0.69 mmol/L和1.14 mmol/L。在暴露于H2O2 12小时后，H2O2处理的野生型CHO细胞和TREK-1/CHO细胞的IC(50)值分别为0.07 mmol/L和0.09 mmol/L。此外，SNP/H2O2诱导TREK-1/CHO细胞凋亡的程度低于野生型CHO细胞（P<0.05）。
结果表明TREK-1对氧化损伤起到保护作用。
