Probucol attenuates hyperoxia-induced lung injury in mice.
Hyperoxic lung injury is pathologically characterized by alveolar edema, interlobular septal edema, hyaline membrane disease, lung inflammation, and alveolar hemorrhage. Although the precise mechanism by which hyperoxia causes lung injury is not well defined, oxidative stress, epithelial cell death,...
| Main Authors: | , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2017-01-01
|
| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC5383131?pdf=render |
| _version_ | 1811330988138037248 |
|---|---|
| author | Tomonobu Kawaguchi Toyoshi Yanagihara Tetsuya Yokoyama Saiko Suetsugu-Ogata Naoki Hamada Chika Harada-Ikeda Kunihiro Suzuki Takashige Maeyama Kazuyoshi Kuwano Yoichi Nakanishi |
| author_facet | Tomonobu Kawaguchi Toyoshi Yanagihara Tetsuya Yokoyama Saiko Suetsugu-Ogata Naoki Hamada Chika Harada-Ikeda Kunihiro Suzuki Takashige Maeyama Kazuyoshi Kuwano Yoichi Nakanishi |
| author_sort | Tomonobu Kawaguchi |
| collection | DOAJ |
| description | Hyperoxic lung injury is pathologically characterized by alveolar edema, interlobular septal edema, hyaline membrane disease, lung inflammation, and alveolar hemorrhage. Although the precise mechanism by which hyperoxia causes lung injury is not well defined, oxidative stress, epithelial cell death, and proinflammatory cytokines are thought to be involved. Probucol-a commercially available drug for treating hypercholesterolemia-has been suggested to have antioxidant and antiapoptotic effects. This study aimed to assess whether probucol could attenuate hyperoxic lung injury in mice. Mice were exposed to 95% O2 for 72 h, with or without pre-treatment with 130 μg/kg probucol intratracheally. Probucol treatment significantly decreased both the number of inflammatory cells in the bronchoalveolar lavage fluid and the degree of lung injury in hyperoxia-exposed mice. Probucol treatment reduced the number of cells positive for 8-hydroxyl-2'-deoxyguanosine or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and suppressed NF-κB activation, Bax expression, and caspase-9 activation in lung tissues from hyperoxia-exposed mice. These results suggest that probucol can reduce oxidative DNA damage, apoptotic cell death, and inflammation in lung tissues. Intratracheal administration of probucol may be a novel treatment for lung diseases induced by oxidative stress, such as hyperoxic lung injury and acute respiratory distress syndrome. |
| first_indexed | 2024-04-13T16:11:07Z |
| format | Article |
| id | doaj.art-915c483565b54b579ffa850d5a4912ed |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-13T16:11:07Z |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-915c483565b54b579ffa850d5a4912ed2022-12-22T02:40:14ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01124e017512910.1371/journal.pone.0175129Probucol attenuates hyperoxia-induced lung injury in mice.Tomonobu KawaguchiToyoshi YanagiharaTetsuya YokoyamaSaiko Suetsugu-OgataNaoki HamadaChika Harada-IkedaKunihiro SuzukiTakashige MaeyamaKazuyoshi KuwanoYoichi NakanishiHyperoxic lung injury is pathologically characterized by alveolar edema, interlobular septal edema, hyaline membrane disease, lung inflammation, and alveolar hemorrhage. Although the precise mechanism by which hyperoxia causes lung injury is not well defined, oxidative stress, epithelial cell death, and proinflammatory cytokines are thought to be involved. Probucol-a commercially available drug for treating hypercholesterolemia-has been suggested to have antioxidant and antiapoptotic effects. This study aimed to assess whether probucol could attenuate hyperoxic lung injury in mice. Mice were exposed to 95% O2 for 72 h, with or without pre-treatment with 130 μg/kg probucol intratracheally. Probucol treatment significantly decreased both the number of inflammatory cells in the bronchoalveolar lavage fluid and the degree of lung injury in hyperoxia-exposed mice. Probucol treatment reduced the number of cells positive for 8-hydroxyl-2'-deoxyguanosine or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and suppressed NF-κB activation, Bax expression, and caspase-9 activation in lung tissues from hyperoxia-exposed mice. These results suggest that probucol can reduce oxidative DNA damage, apoptotic cell death, and inflammation in lung tissues. Intratracheal administration of probucol may be a novel treatment for lung diseases induced by oxidative stress, such as hyperoxic lung injury and acute respiratory distress syndrome.http://europepmc.org/articles/PMC5383131?pdf=render |
| spellingShingle | Tomonobu Kawaguchi Toyoshi Yanagihara Tetsuya Yokoyama Saiko Suetsugu-Ogata Naoki Hamada Chika Harada-Ikeda Kunihiro Suzuki Takashige Maeyama Kazuyoshi Kuwano Yoichi Nakanishi Probucol attenuates hyperoxia-induced lung injury in mice. PLoS ONE |
| title | Probucol attenuates hyperoxia-induced lung injury in mice. |
| title_full | Probucol attenuates hyperoxia-induced lung injury in mice. |
| title_fullStr | Probucol attenuates hyperoxia-induced lung injury in mice. |
| title_full_unstemmed | Probucol attenuates hyperoxia-induced lung injury in mice. |
| title_short | Probucol attenuates hyperoxia-induced lung injury in mice. |
| title_sort | probucol attenuates hyperoxia induced lung injury in mice |
| url | http://europepmc.org/articles/PMC5383131?pdf=render |
| work_keys_str_mv | AT tomonobukawaguchi probucolattenuateshyperoxiainducedlunginjuryinmice AT toyoshiyanagihara probucolattenuateshyperoxiainducedlunginjuryinmice AT tetsuyayokoyama probucolattenuateshyperoxiainducedlunginjuryinmice AT saikosuetsuguogata probucolattenuateshyperoxiainducedlunginjuryinmice AT naokihamada probucolattenuateshyperoxiainducedlunginjuryinmice AT chikaharadaikeda probucolattenuateshyperoxiainducedlunginjuryinmice AT kunihirosuzuki probucolattenuateshyperoxiainducedlunginjuryinmice AT takashigemaeyama probucolattenuateshyperoxiainducedlunginjuryinmice AT kazuyoshikuwano probucolattenuateshyperoxiainducedlunginjuryinmice AT yoichinakanishi probucolattenuateshyperoxiainducedlunginjuryinmice |