Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 16، دوره 18، شماره 1، فروردین 2015، صفحه 98-103 اصل مقاله (1.29 M) | ||
| نوع مقاله: Retraction | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2015.3895 | ||
| نویسندگان | ||
| Shouli Yu* 1؛ Min Shi2؛ Qinghui Liu2؛ Changting Liu2؛ Jun Guo2؛ Senyang Yu2؛ Tingshu Jiang3 | ||
| 1Department of quality management, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai City, Shandong Province, China | ||
| 2Department of Nanlou, Respiratory Disease, Chinese PLA General Hospital, Beijing, China | ||
| 3Respiratory Department, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai City, Shandong Province, China | ||
| چکیده | ||
| Objective(s):Therapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury, the exact mechanisms are still less known in the hyperoxic acute lung injury (HALI). Materials and Methods: In this study, we investigated the time course changes of oxidative stress and inflammation in lung tissues of rats exposed to >95% oxygen for 12-60 hr. Results: We found that at 12 hr after hyperoxia challenge, the activities of superoxide dismutase and glutathione peroxidase were significantly reduced with remarkably increased lipid peroxidation. At 12 hr, NF-κB p65 expression was also upregulated, but Iκ-Bα expression showed a remarkable decline. Significant production of inflammatory mediators, e.g, interleukin-1β, occurred 24 hr after hyperoxia exposure. In addition, the expression of intracellular adhesion molecule 1 expression and the activity of myeloperoxidase were significantly increased at 24 hr with a peak at 48 hr. Conclusion: Our data support that hyperoxia-induced oxidative damage and NF-κB pathway activation implicate in the early phase of HALI pathogenesis. | ||
| کلیدواژهها | ||
| Acute lung injury؛ Hyperoxia؛ Inflammation؛ Oxidative stress | ||
| مراجع | ||
|
1. Dang H, Yang L, Wang S, Fang F, Xu F. Calcitonin gene-related peptide ameliorates hyperoxia-induced lung injury in neonatal rats. Tohoku J Exp Med 2012; 227:129-138.
2. Fok TF, Gu GJ, To KF, Xu F, Ng PC, Yin J. Oxygen consumption by lungs with acute and chronic injury in a rabbit model. Intensive Care Med 2001; 27:1532-1538.
3. Saugstad OD. Mechanisms of tissue injury by oxygen radicals: implications for neonatal disease. Acta Paediatr 1996; 85:1-4.
4. Tao W, Shu YS, Miao QB, Zhu YB. Attenuation of hyperoxia-induced lung injury in rats by adrenomedullin. Inflammation 2012; 35:150-157.
5. Xu F, Fok TF, Yin J. Hyperoxia-induced lung injury in premature rat: description of a suitable model for the study of lung diseases in newborns. Chin Med J 1998; 111:619-624.
6. Chen ZT, Li SL, Cai EQ, Wu WL, Jin JS, Zhu B. LPS induces pulmonary intravascular macrophages producing inflammatory mediators via activating NF-kappaB. J Cell Biochem 2003; 89:1206-1214.
7. Jungraithmayr W, Jang JH, Schrepfer S, Inci I, Weder W. Small animal models of experimental obliterative bronchiolitis. Am J Respir Cell Mol Biol 2013; 48:675-684.
8. Porzionato A, Zaramella P, Macchi V, Sarasin G, Di Giulio C, Rigon A, et al. Cyclosporine and hyperoxia-induced lung damage in neonatal rats. Respir Physiol Neurobiol 2013; 187:41-46.
9. Samareh Fekri M, Poursalehi HR, Najafipour H, Dabiri S, Shokoohi M, Siahposht Khacheki A, et al. Pulmonary complications of gastric fluid and bile salts aspiration, an experimental study in rat. Iran J Basic Med Sci 2013; 16:790-796. 10. Pryor WA, Godber SS. Noninvasive measures of oxidative stress status in humans. Free Radic Biol Med 1991; 10:177-184.
11. Cochrane CG. Cellular injury by oxidants. Am J Med 1991; 91:23S-30S.
12. Haddad JJ. Science review: redox and oxygen-sensitive transcription factors in the regulation of oxidant-mediated lung injury: role for hypoxia-inducible factor-1alpha. Critic Care 2003; 7:47-54.
13. Chollet-Martin S, Jourdain B, Gibert C, Elbim C, Chastre J, Gougerot-Pocidalo MA. Interactions between neutrophils and cytokines in blood and alveolar spaces during ARDS. Am J Respir Critic Care Med 1996; 154:594-601.
14. Pittet JF, Mackersie RC, Martin TR, Matthay MA. Biological markers of acute lung injury: prognostic and pathogenetic significance. Am J Respir Critic Care Med 1997; 155:1187-1205.
15. D'Angio CT, LoMonaco MB, Chaudhry SA, Paxhia A, Ryan RM. Discordant pulmonary proinflammatory cytokine expression during acute hyperoxia in the newborn rabbit. Exp lung Res 1999; 25:443-465.
16. Desmarquest P, Chadelat K, Corroyer S, Cazals V, Clement A. Effect of hyperoxia on human macrophage cytokine response. Respir Med 1998; 92:951-960.
17. Horinouchi H, Wang CC, Shepherd KE, Jones R. TNF alpha gene and protein expression in alveolar macrophages in acute and chronic hyperoxia-induced lung injury. Am J Respir Cell Mol Biol 1996; 14:548-555.
18. Nathens AB, Bitar R, Watson RW, Issekutz TB, Marshall JC, Dackiw AP, et al. Thiol-mediated regulation of ICAM-1 expression in endotoxin-induced acute lung injury. J Immunol 1998; 160:2959-2966.
19. Boxer LA, Axtell R, Suchard S. The role of the neutrophil in inflammatory diseases of the lung. Blood Cells 1990; 16:25-40. | ||
|
آمار تعداد مشاهده مقاله: 2,488 تعداد دریافت فایل اصل مقاله: 1,538 |
||