OBJECTIVE: To investigate the effects of emodin on aquaporin 5 (AQP5) expression in rats with sepsis-induced acute lung injury. METHODS: We divided 60 adult male Sprague-Dawley rats, weighing 200-230 g, into four groups: control, sham surgery, model and emodin groups (n = 15 for each). We created a sepsis model with cecal ligation and puncture; the sham surgery group had their cecums replaced after exposure outside the abdominal cavity. Each group was further divided into three subgroups (n = 5 for each) and expressions of AQP5 mRNA and proteins in lung tissue were measured by real-time fluorescence polymerase chain reaction and western blot at 6,12 and 24 h after surgery. RESULTS: AQP5 expression did not change over time in the control group and sham surgery group, but decreased over time in the model group. The lowest expression was found in 12-h subgroup, which significantly differed from the 6-h subgroup (P < 0.01). Compared with the model group, AQP5 expression in the emodin group was significantly higher in all the subgroups (all P < 0.01). Expressions in the 12-h subgroup were the highest, and significantly differed from the other subgroups. We found that lung tissue damage, such as pulmonary edema, alveolar damage and the exudation of red blood cells in pulmonary interstitium and alveolar, was significantly milder in the emodin group under light microscope than the model group. CONCLUSION: AQP5 expression was significantly down-regulated in rats with sepsis-induced acute lung injury induced by cecal ligation and puncture. Early prophylactic use of emodin can significantly enhance the AQP5 expression, thus effectively reducing the degree of pulmonary edema in septic rats.
OBJECTIVE: To investigate the effects of emodin on aquaporin 5 (AQP5) expression in rats with sepsis-induced acute lung injury. METHODS: We divided 60 adult male Sprague-Dawley rats, weighing 200-230 g, into four groups: control, sham surgery, model and emodin groups (n = 15 for each). We created a sepsis model with cecal ligation and puncture; the sham surgery group had their cecums replaced after exposure outside the abdominal cavity. Each group was further divided into three subgroups (n = 5 for each) and expressions of AQP5 mRNA and proteins in lung tissue were measured by real-time fluorescence polymerase chain reaction and western blot at 6,12 and 24 h after surgery. RESULTS:AQP5 expression did not change over time in the control group and sham surgery group, but decreased over time in the model group. The lowest expression was found in 12-h subgroup, which significantly differed from the 6-h subgroup (P < 0.01). Compared with the model group, AQP5 expression in the emodin group was significantly higher in all the subgroups (all P < 0.01). Expressions in the 12-h subgroup were the highest, and significantly differed from the other subgroups. We found that lung tissue damage, such as pulmonary edema, alveolar damage and the exudation of red blood cells in pulmonary interstitium and alveolar, was significantly milder in the emodin group under light microscope than the model group. CONCLUSION:AQP5 expression was significantly down-regulated in rats with sepsis-induced acute lung injury induced by cecal ligation and puncture. Early prophylactic use of emodin can significantly enhance the AQP5 expression, thus effectively reducing the degree of pulmonary edema in septic rats.