Yun-Zhi Ling1, Xiao-Hong Li1, Li Yu2, Ye Zhang3, Qi-Sheng Liang1, Xiao-di Yang4, Hong-Tao Wang5. 1. Department of Anesthesiology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, China. 2. Department of Laboratory Medicine, Bengbu Medical College, Bengbu 233030, China. 3. Department of Anesthesiology, Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China. 4. Department of Parasitology, Bengbu Medical College, Bengbu 233030, China. 5. Department of Immunology, Bengbu Medical College, Bengbu 233030, China.
Abstract
OBJECTIVE: To investigate the protective effects of parecoxib from oxidative stress induced by hydrogen peroxide (H2O2) in rat astrocytes in vitro. METHODS: All experiments included 4 groups: (1) negative control (NC) group, without any treatment; (2) H2O2 treatment group, 100 μmol/L H2O2 treatment for 24 h; (3) and (4) parecoxib pretreatment groups, 80 and 160 μmol/L parecoxib treatment for 24 h, respectively, and then treated with 100 μmol/L H2O2. Several indices were investigated, and the expressions of Bax, Bcl-2, and brain-derived neurotrophic factor (BDNF) were quantified. RESULTS: Compared to the NC group, exposure to H2O2 resulted in significant morphological changes, which could be reversed by pretreatment of parecoxib. In addition, H2O2 treatment led to loss of viability (P=0.026) and increased intracellular reactive oxygen species (ROS) levels (P<0.001), and induced apoptosis (P<0.01) in the primary astrocytes relative to the NC group. However, in the parecoxib pretreatment groups, all the above changes reversed significantly (P<0.05) as compared to the H2O2 treatment group, and were nearly unchanged when compared to the NC group. Mechanical investigation showed that dysregulated Bax, Bcl-2, and BDNF could be implicated in these changes. CONCLUSIONS: Our results indicated that parecoxib provided a protective effect from oxidative stress induced by exposure to H2O2.
OBJECTIVE: To investigate the protective effects of parecoxib from oxidative stress induced by hydrogen peroxide (H2O2) in rat astrocytes in vitro. METHODS: All experiments included 4 groups: (1) negative control (NC) group, without any treatment; (2) H2O2 treatment group, 100 μmol/L H2O2 treatment for 24 h; (3) and (4) parecoxib pretreatment groups, 80 and 160 μmol/L parecoxib treatment for 24 h, respectively, and then treated with 100 μmol/L H2O2. Several indices were investigated, and the expressions of Bax, Bcl-2, and brain-derived neurotrophic factor (BDNF) were quantified. RESULTS: Compared to the NC group, exposure to H2O2 resulted in significant morphological changes, which could be reversed by pretreatment of parecoxib. In addition, H2O2 treatment led to loss of viability (P=0.026) and increased intracellular reactive oxygen species (ROS) levels (P<0.001), and induced apoptosis (P<0.01) in the primary astrocytes relative to the NC group. However, in the parecoxib pretreatment groups, all the above changes reversed significantly (P<0.05) as compared to the H2O2 treatment group, and were nearly unchanged when compared to the NC group. Mechanical investigation showed that dysregulated Bax, Bcl-2, and BDNF could be implicated in these changes. CONCLUSIONS: Our results indicated that parecoxib provided a protective effect from oxidative stress induced by exposure to H2O2.
Authors: Fadi N Salloum; Nicholas N Hoke; Ignacio M Seropian; Amit Varma; Evan D Ownby; Jon-Erik Houser; Benjamin W Van Tassell; Antonio Abbate Journal: J Cardiovasc Pharmacol Date: 2009-06 Impact factor: 3.105