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