Anesthetic Isoflurane Posttreatment Attenuates Experimental Lung Injury by Inhibiting Inflammation and Apoptosis. (17th April 2013)
- Record Type:
- Journal Article
- Title:
- Anesthetic Isoflurane Posttreatment Attenuates Experimental Lung Injury by Inhibiting Inflammation and Apoptosis. (17th April 2013)
- Main Title:
- Anesthetic Isoflurane Posttreatment Attenuates Experimental Lung Injury by Inhibiting Inflammation and Apoptosis
- Authors:
- Li, Jun-tang
Wang, Hui
Li, Wei
Wang, Li-feng
Hou, Li-chao
Mu, Jing-lan
Liu, Xin
Chen, Hui-juan
Xie, Ke-lang
Li, Nan-lin
Gao, Chun-fang - Other Names:
- Fantuzzi Giamila Academic Editor.
- Abstract:
- Abstract : We investigated the effect of 1.4% isoflurane (ISO) on the development of inflammation and apoptosis caused by zymosan (ZY) in mice. We found that ZY-challenged mice exhibited significant body weight loss, markedly high mortality, and significant lung injury characterized by the deterioration of histopathology, histologic scores, and wet-to-dry ratio after ISO treatment. ISO dramatically attenuated ZY-induced lung neutrophil recruitment and inflammation, as evidenced by the reduced levels of total cells, neutrophils, and proinflammatory cytokines (i.e., tumor necrosis factor- α, interleukin- (IL-) 1 β, IL-6, and macrophage inflammatory protein-2) in bronchoalveolar lavage fluid and of their mRNA expression in lung tissues. ISO also inhibited ZY-induced expression and activation of nuclear factor-kappaB p65 and inducible nitric oxide synthase in pulmonary tissue. ZY administration also resulted in the upregulation of heme oxygenase-1 expression and activity in the lung, which was further enhanced by ISO treatment. Moreover, ISO markedly prevented ZY-induced pulmonary cell apoptosis in mice, as reflected by the decrease in expression of procaspase-8, procaspase-3, cleaved caspase-8, and cleaved caspase-3, as well as in caspase-3 activity and Bcl-2-associated X/B-cell lymphoma 2 ratio. These results indicate that ISO is a potential therapeutic drug for treating ZY-induced lung injury, and further investigations are warranted.
- Is Part Of:
- Mediators of inflammation. Volume 2013(2013)
- Journal:
- Mediators of inflammation
- Issue:
- Volume 2013(2013)
- Issue Display:
- Volume 2013, Issue 2013 (2013)
- Year:
- 2013
- Volume:
- 2013
- Issue:
- 2013
- Issue Sort Value:
- 2013-2013-2013-0000
- Page Start:
- Page End:
- Publication Date:
- 2013-04-17
- Subjects:
- Inflammation -- Mediators -- Periodicals
Biological response modifiers -- Periodicals
Inflammation (Pathologie) -- Médiateurs
Immunomodulateurs
Biological response modifiers
Inflammation -- Mediators
Immunology
Autacoids
Immunologic Factors
Cell Adhesion Molecules
Cell Communication
Cytokines
Inflammation
Periodicals
Electronic journals
616.0473 - Journal URLs:
- https://www.hindawi.com/journals/mi/ ↗
- DOI:
- 10.1155/2013/108928 ↗
- Languages:
- English
- ISSNs:
- 0962-9351
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 17106.xml