BACKGROUND: Edaravone (3-methyl-1-penyl-2-pyrazolin-5-one) is a potent free-radical scavenger and has the antioxidant ability to inhibit lipid peroxidation. The study aimed to examine the effect of edaravone on protecting the acute injury of human type II alveolar epithelial cells (A549 cells) induced by paraquat (PQ) and the change of production of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD). METHODS: A549 cells were cultured and divided into PQ group (group P), edaravone-treated group (group E) and normal control group (group C). The cells in group P were exposed to paraquat (600 μmol/L), and the cells in group E were treated with edaravone (100 μmol/L) additionally, and no drug intervention was given to the cells in group C. Real-time monitoring by LSCM was used to detect the cell response and the intracellular dynamic change of ROS level in A549 cells after administration of PQ and edaravone. And the levels of SOD and MDA were detected respectively by biochemistry colorimetry. Data were expressed as mean ± standard error of the mean. Statistical analysis was carried out with the soft SPSS 16.0. RESULTS: The concentration of intracellular ROS significantly increased when PQ was given to A549 cells. But after administration of edaravone, the concentration of intracellular ROS was decreased. Compared to the PQ group, the levels of SOD in the edaravone group were significantly increased while the levels of MDA were markedly decreased. CONCLUSIONS: Paraquat can increase the oxidative stress, and induce the lipid peroxidation of A549 cells. Edaravone has the effect to scavenge reactive oxygen species, and to protect against the PQ-induced lung toxicity.
BACKGROUND:Edaravone (3-methyl-1-penyl-2-pyrazolin-5-one) is a potent free-radical scavenger and has the antioxidant ability to inhibit lipid peroxidation. The study aimed to examine the effect of edaravone on protecting the acute injury of human type II alveolar epithelial cells (A549 cells) induced by paraquat (PQ) and the change of production of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD). METHODS: A549 cells were cultured and divided into PQ group (group P), edaravone-treated group (group E) and normal control group (group C). The cells in group P were exposed to paraquat (600 μmol/L), and the cells in group E were treated with edaravone (100 μmol/L) additionally, and no drug intervention was given to the cells in group C. Real-time monitoring by LSCM was used to detect the cell response and the intracellular dynamic change of ROS level in A549 cells after administration of PQ and edaravone. And the levels of SOD and MDA were detected respectively by biochemistry colorimetry. Data were expressed as mean ± standard error of the mean. Statistical analysis was carried out with the soft SPSS 16.0. RESULTS: The concentration of intracellular ROS significantly increased when PQ was given to A549 cells. But after administration of edaravone, the concentration of intracellular ROS was decreased. Compared to the PQ group, the levels of SOD in the edaravone group were significantly increased while the levels of MDA were markedly decreased. CONCLUSIONS:Paraquat can increase the oxidative stress, and induce the lipid peroxidation of A549 cells. Edaravone has the effect to scavenge reactive oxygen species, and to protect against the PQ-induced lung toxicity.