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TREK-1对硝普钠和过氧化氢诱导的氧化损伤的保护作用。

Protective effects of TREK-1 against oxidative injury induced by SNP and H2O2.

作者信息

Sun Li-na, Li Liao-liao, Li Zheng-bin, Wang Ling, Wang Xiao-liang

机构信息

Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

出版信息

Acta Pharmacol Sin. 2008 Oct;29(10):1150-6. doi: 10.1111/j.1745-7254.2008.00853.x.

Abstract

AIM

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.

METHODS

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.

RESULTS

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).

CONCLUSION

The results demonstrated that TREK-1 played a protective role against oxidative injury.

摘要

目的

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。

方法

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。

结果

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)。

结论

结果表明TREK-1对氧化损伤起到保护作用。

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