Hui Xie1, Ruilan Wang, Xue Tang, Ying Xiong, Rong Xu, Xin Wu. 1. Department of Critical Care Medicine, Affiliated First People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200080, China.
Abstract
AIM: To investigate the starting point of paraquat-induced pulmonary fibrosis in rats. MATERIALS & METHODS: A total of 96 healthy Sprague-Dawley rats were randomly divided into eight groups (n = 12 in each group) including a control and paraquat-poisoning group. Control rats received treatment with saline. Samples were collected at 2, 6, 12, 24, 48, 72 and 120 h after paraquat administered by lavage. All lung tissues were stained with hematoxylin-eosin and Masson's trichrome. Collagen III expressed in bronchoalveolar lavage fluid was detected by ELISA. The α-smooth muscle actin in lung tissue was detected by western blotting. RESULTS: A rat model of paraquat poisoning was established. Histological examination results indicated that lung fibrosis started in rats 2 h after paraquat poisoning. Compared with the control group, the collagen III protein in bronchoalveolar lavage fluid was significantly upregulated in the 2-h group (α = 0.05) and the same level was maintained in the other poisoning groups. The expression of α-smooth muscle actin in the lung tissue was significantly increased in the 12-h group (α = 0.05) and remained at the same level after 12 h. CONCLUSION: The paraquat-induced pulmonary fibrosis in rats began at an early stage of inflammation. The therapy of antifibrosis should be applied at an early time of paraquat poisoning.
AIM: To investigate the starting point of paraquat-induced pulmonary fibrosis in rats. MATERIALS & METHODS: A total of 96 healthy Sprague-Dawley rats were randomly divided into eight groups (n = 12 in each group) including a control and paraquat-poisoning group. Control rats received treatment with saline. Samples were collected at 2, 6, 12, 24, 48, 72 and 120 h after paraquat administered by lavage. All lung tissues were stained with hematoxylin-eosin and Masson's trichrome. Collagen III expressed in bronchoalveolar lavage fluid was detected by ELISA. The α-smooth muscle actin in lung tissue was detected by western blotting. RESULTS: A rat model of paraquatpoisoning was established. Histological examination results indicated that lung fibrosis started in rats 2 h after paraquatpoisoning. Compared with the control group, the collagen III protein in bronchoalveolar lavage fluid was significantly upregulated in the 2-h group (α = 0.05) and the same level was maintained in the other poisoning groups. The expression of α-smooth muscle actin in the lung tissue was significantly increased in the 12-h group (α = 0.05) and remained at the same level after 12 h. CONCLUSION: The paraquat-induced pulmonary fibrosis in rats began at an early stage of inflammation. The therapy of antifibrosis should be applied at an early time of paraquatpoisoning.