Bing Wan1, Wu-Jian Xu2, Ping Zhan2, Jia-Jia Jin2, Guang-Min Xi2, Mei-Zi Chen2, Yang-Bo Hu2, Su-Hua Zhu2, Hong-Bing Liu2, Xiao-Xia Wang2, Xiu-Wei Zhang3, Tang-Feng Lv4, Yong Song5. 1. Department of Respiratory and Critical Medicine, Jinling Hospital, Nanjing Clinical School of Southern Medical University (Guangzhou), Nanjing 210002, China; Department of Respiratory Medicine, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing 210002, China. 2. Department of Respiratory and Critical Medicine, Jinling Hospital, Nanjing Clinical School of Southern Medical University (Guangzhou), Nanjing 210002, China. 3. Department of Respiratory Medicine, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing 210002, China. 4. Department of Respiratory and Critical Medicine, Jinling Hospital, Nanjing Clinical School of Southern Medical University (Guangzhou), Nanjing 210002, China. Electronic address: bairoushui@163.com. 5. Department of Respiratory and Critical Medicine, Jinling Hospital, Nanjing Clinical School of Southern Medical University (Guangzhou), Nanjing 210002, China. Electronic address: Yong_song6310@yahoo.com.
Abstract
OBJECTIVE: We investigated the effect of topotecan on injury and inflammation in a model of ventilator-inducedlunginjury (VILI). METHODS: Acute lung injury (ALI) was induced in mice by high-tidal volume ventilation, and the mice were then treated with topotecan or PBS. Lung tissue and bronchoalveolar lavage fluid were collected to assess pulmonary vascular leaks, inflammation, and cell apoptosis. RESULTS: Compared to PBS treatment, topotecan significantly decreased the ALI score, myeloperoxidase (MPO) content, total protein concentration, and presence of inflammatory cells and inflammatory cytokines in bronchoalveolar lavage fluid. Topotecan also reduced caspase-3 activation and type Ⅱ alveolar epithelial cell apoptosis. Moreover, topotecan inhibited NF-κB expression and activation in the VILI model. CONCLUSION: Topotecan alleviates acute lung injury in the model of VILI through the inhibition of the NF-κB pathway.
OBJECTIVE: We investigated the effect of topotecan on injury and inflammation in a model of ventilator-inducedlunginjury (VILI). METHODS:Acute lung injury (ALI) was induced in mice by high-tidal volume ventilation, and the mice were then treated with topotecan or PBS. Lung tissue and bronchoalveolar lavage fluid were collected to assess pulmonary vascular leaks, inflammation, and cell apoptosis. RESULTS: Compared to PBS treatment, topotecan significantly decreased the ALI score, myeloperoxidase (MPO) content, total protein concentration, and presence of inflammatory cells and inflammatory cytokines in bronchoalveolar lavage fluid. Topotecan also reduced caspase-3 activation and type Ⅱ alveolar epithelial cell apoptosis. Moreover, topotecan inhibited NF-κB expression and activation in the VILI model. CONCLUSION:Topotecan alleviates acute lung injury in the model of VILI through the inhibition of the NF-κB pathway.