,Protective effects of TREK-1 against oxidative injury induced by SNP and H2O21

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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-y1)-2,5-diphenyltetrazolium bromide (MTT) assay in the presence of sodium nitroprusside (SNP) or hydrogen peroxide (H2O2).Apoptosis of wild-type CHO and TREK-I/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-I/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.
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