Open AccessProtective effects of TREK‐1 against oxidative injury induced by SNP and H 2 O 2 1
Author(s) -
SUN Lina,
LI Liaoliao,
LI Zhengbin,
WANG Ling,
WANG Xiaoliang
Publication year - 2008
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2008.00853.x
Subject(s) - chinese hamster ovary cell , microbiology and biotechnology , apoptosis , wild type , hydrogen peroxide , chemistry , oxidative stress , cell culture , sodium nitroprusside , biology , biochemistry , nitric oxide , endocrinology , mutant , genetics , gene
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 (H 2 O 2 ). Apoptosis of wild‐type CHO and TREK‐1/CHO cells was detected using Hoechst33342 staining. Results: Both SNP and H 2 O 2 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 H 2 O 2 ‐treated wild‐type CHO and TREK‐1/CHO cells, respectively, following 12 h exposure to H 2 O 2 . Moreover, SNP/H 2 O 2 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.