| Autor: |
Li-na SUN, Liao-liao LI, Zheng-bin LI, Ling WANG, Xiao-liang WANG |
| Předmět: |
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| Zdroj: |
Acta Pharmacologica Sinica; Oct2008, Vol. 29 Issue 10, p1150-1156, 7p, 2 Color Photographs, 1 Diagram, 2 Graphs |
| Abstrakt: |
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 (IC50) values for wild-type CHO and TREK-1/CHO cells were calculated as 0.69 mmol/L and 1.14 mmol/L, respectively. The IC50 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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