Objective To investigate the effect of hyperbaric oxygen ( HBO ) combined with temozolomide (TMZ) on the apoptosis of glioma U373MG cells and also to explore possible mechanism involved. Methods Upon completion of cell culture, they were divided into 4 groups, i. e. the control group, the TMZ group, the HBO group and the HBO + TMZ group. The control group received neither HBO nor drug treatment, the TMZ group only received 50μmol/L TMZ, the HBO group just received 0. 24 MPa HBO treatment for 3 hours and the HBO + TMZ group was given 50μmol/L TMZ 3 hours after HBO pretreatment. CCK-8 method was used to detect the effects of HBO and TMZ alone or combined use of 2 treatment methods on the proliferation of glioma U373MG cells. Flow cytometry was used to detect HBO and TMZ alone or combined use of 2 treatment methods on glioma U373MG cells and changes in the level of reactive oxygen species (ROS). Western blotting was used to detect the expression of U373MG apoptosis-related proteins. Results The proliferation inhibition of U373MG cells in the HBO+TMZ group was more obvious as compared with that of the TMZ group(P<0. 05). U373MG cells in the TMZ group showed early and late apoptosis, the rate of apoptosis in the HBO +TMZ group was significantly higher than that of the control group [(73. 19 ± 3. 58)％ vs. (30. 5 ± 2. 27)％] (P<0. 01). As compared with the blank control and HBO groups, the expression level of Bcl-2 in the TMZ group significantly decreased, while the expression level of Bax and caspase-3 markedly increased. Furthermore, more obvious changes could be detected, when the HBO+TMZ group was compared with the TMZ group(P<0. 05 or P<0. 01). ROS level in the U373MG cells of the HBO +TMZ group obviously increased(P <0. 01). With the addition of ROS scavenger NAC, apoptosis was inhibited in the HBO+TMZ group(P<0. 01). Conclusion HBO combined with TMZ could enhance the inhibitory effect of TMZ on the proliferation of U373MG cells, and promote apoptosis induced by TMZ through up-regulating ROS levels in U373MG cells.

Objective To investigate the effect of hyperbaric oxygen ( HBO ) combined with temozolomide (TMZ) on the apoptosis of glioma U373MG cells and also to explore possible mechanism involved. Methods Upon completion of cell culture, they were divided into 4 groups, i. e. the control group, the TMZ group, the HBO group and the HBO + TMZ group. The control group received neither HBO nor drug treatment, the TMZ group only received 50μmol/L TMZ, the HBO group just received 0. 24 MPa HBO treatment for 3 hours and the HBO + TMZ group was given 50μmol/L TMZ 3 hours after HBO pretreatment. CCK-8 method was used to detect the effects of HBO and TMZ alone or combined use of 2 treatment methods on the proliferation of glioma U373MG cells. Flow cytometry was used to detect HBO and TMZ alone or combined use of 2 treatment methods on glioma U373MG cells and changes in the level of reactive oxygen species (ROS). Western blotting was used to detect the expression of U373MG apoptosis-related proteins. Results The proliferation inhibition of U373MG cells in the HBO+TMZ group was more obvious as compared with that of the TMZ group(P<0. 05). U373MG cells in the TMZ group showed early and late apoptosis, the rate of apoptosis in the HBO +TMZ group was significantly higher than that of the control group [(73. 19 ± 3. 58)％ vs. (30. 5 ± 2. 27)％] (P<0. 01). As compared with the blank control and HBO groups, the expression level of Bcl-2 in the TMZ group significantly decreased, while the expression level of Bax and caspase-3 markedly increased. Furthermore, more obvious changes could be detected, when the HBO+TMZ group was compared with the TMZ group(P<0. 05 or P<0. 01). ROS level in the U373MG cells of the HBO +TMZ group obviously increased(P <0. 01). With the addition of ROS scavenger NAC, apoptosis was inhibited in the HBO+TMZ group(P<0. 01). Conclusion HBO combined with TMZ could enhance the inhibitory effect of TMZ on the proliferation of U373MG cells, and promote apoptosis induced by TMZ through up-regulating ROS levels in U373MG cells.