Y Song1, B Mao, G Qian. 1. Department of Respiratory Medicine, Nanjing General Hospital of Nanjing Command, Nanjing 210002.
Abstract
OBJECTIVE: To evaluate the effects of apoptosis and expression of apoptotic related genes on acute respiratory distress syndrome (ARDS). METHODS: Nine patients with ARDS and 5 non-ARDS patients were included. By using TUNEL, histopathology and immunocytochemistry techniques, apoptosis and Fas, FasL protein expression were studied in patients with ARDS in acute stage and in control subjects. RESULTS: Apoptosis ratio was significantly higher in lung tissues in the patients with ARDS than in those of control subjects, especially in alveolar epithelial cells and pulmonary vascular endothelial cells. Fas, FasL protein expression were up-regulated in lung tissues of patients with ARDS. There was a significant correlation between expression of Fas, FasL and ratio of apoptosis. CONCLUSIONS: During the acute stage of ARDS, increase of apoptosis ratio in alveolar epithelial cells and pulmonary vascular endothelial cells, and activation of Fas/FasL system may contribute to the pathogenesis of this syndrome.
OBJECTIVE: To evaluate the effects of apoptosis and expression of apoptotic related genes on acute respiratory distress syndrome (ARDS). METHODS: Nine patients with ARDS and 5 non-ARDS patients were included. By using TUNEL, histopathology and immunocytochemistry techniques, apoptosis and Fas, FasL protein expression were studied in patients with ARDS in acute stage and in control subjects. RESULTS: Apoptosis ratio was significantly higher in lung tissues in the patients with ARDS than in those of control subjects, especially in alveolar epithelial cells and pulmonary vascular endothelial cells. Fas, FasL protein expression were up-regulated in lung tissues of patients with ARDS. There was a significant correlation between expression of Fas, FasL and ratio of apoptosis. CONCLUSIONS: During the acute stage of ARDS, increase of apoptosis ratio in alveolar epithelial cells and pulmonary vascular endothelial cells, and activation of Fas/FasL system may contribute to the pathogenesis of this syndrome.