Effect of selective versus non-selective cyclooxygenase inhibitors on ischemia-reperfusion-induced hepatic injury in rats
Ischemia-reperfusion (IR) injury represents an important pathological process of liver injury during major hepatic surgery. The role of cyclooxygenase (COX) enzymes in the pathogenesis of ischemia-reperfusion (IR)-induced liver injury is not clear. This study investigated the effect of a selective COX-2 inhibitor, celecoxib, versus non-selective, indomethacin, on hepatic IR injury in rats. Hepatic IR was induced in adult male rats. The animals were divided into 4 groups: normal control (sham group), IR non-treated group; IR-indomethacin-treated group; and IR-celecoxib-treated group. Liver injury was evaluated by serum alanine aminotransferase (ALT) and a histopathological examination of liver tissues. Hepatic tissue content of oxidative stress parameters glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase, malondialdehyde (MDA), nitric oxide (NO) and the inflammatory marker, tumor necrosis factor-alpha, (TNF-α) were measured. Moreover, the immunohistochemical detection of endothelial NO synthase (eNOS), inducible NO synthase (iNOS), and caspase-3 in the hepatic tissue was performed. Celecoxib, but not indomethacin, significantly attenuated hepatic IR injury as evidenced by reduction in serum ALT as well as by improvement in the histopathological scoring. Such effect was associated with attenuation in oxidative stress and TNF-α, along with modulation of immunohistochemical expression of eNOS, iNOS and caspase-3 in the hepatic tissue. The present study concluded that selective COX-2 inhibition (but not non-selective), is hepatoprotective against liver IR injury; indicating a differential role of COX-1 versus COX-2. Modulation of iNOS, eNOS and caspase-3 might participate in the protective effect of selective COX-2-inhibitors..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2015 |
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| Erschienen: |
2015 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:134 |
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| Enthalten in: |
Life sciences - 134(2015), Seite 42-48 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Abdel-Gaber, Seham A [VerfasserIn] |
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| Links: |
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| doi: |
10.1016/j.lfs.2015.04.025 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
OLC1967621713 |
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| 100 | 1 | |a Abdel-Gaber, Seham A |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Effect of selective versus non-selective cyclooxygenase inhibitors on ischemia-reperfusion-induced hepatic injury in rats |
| 264 | 1 | |c 2015 | |
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| 520 | |a Ischemia-reperfusion (IR) injury represents an important pathological process of liver injury during major hepatic surgery. The role of cyclooxygenase (COX) enzymes in the pathogenesis of ischemia-reperfusion (IR)-induced liver injury is not clear. This study investigated the effect of a selective COX-2 inhibitor, celecoxib, versus non-selective, indomethacin, on hepatic IR injury in rats. Hepatic IR was induced in adult male rats. The animals were divided into 4 groups: normal control (sham group), IR non-treated group; IR-indomethacin-treated group; and IR-celecoxib-treated group. Liver injury was evaluated by serum alanine aminotransferase (ALT) and a histopathological examination of liver tissues. Hepatic tissue content of oxidative stress parameters glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase, malondialdehyde (MDA), nitric oxide (NO) and the inflammatory marker, tumor necrosis factor-alpha, (TNF-α) were measured. Moreover, the immunohistochemical detection of endothelial NO synthase (eNOS), inducible NO synthase (iNOS), and caspase-3 in the hepatic tissue was performed. Celecoxib, but not indomethacin, significantly attenuated hepatic IR injury as evidenced by reduction in serum ALT as well as by improvement in the histopathological scoring. Such effect was associated with attenuation in oxidative stress and TNF-α, along with modulation of immunohistochemical expression of eNOS, iNOS and caspase-3 in the hepatic tissue. The present study concluded that selective COX-2 inhibition (but not non-selective), is hepatoprotective against liver IR injury; indicating a differential role of COX-1 versus COX-2. Modulation of iNOS, eNOS and caspase-3 might participate in the protective effect of selective COX-2-inhibitors. | ||
| 540 | |a Nutzungsrecht: Copyright © 2015 Elsevier Inc. All rights reserved. | ||
| 650 | 4 | |a Liver - metabolism | |
| 650 | 4 | |a Alanine Transaminase - blood | |
| 650 | 4 | |a Liver Diseases - blood | |
| 650 | 4 | |a Liver Diseases - drug therapy | |
| 650 | 4 | |a Reperfusion Injury - drug therapy | |
| 650 | 4 | |a Caspase 3 - metabolism | |
| 650 | 4 | |a Liver Diseases - pathology | |
| 650 | 4 | |a Sulfonamides - pharmacology | |
| 650 | 4 | |a Nitric Oxide Synthase Type II - metabolism | |
| 650 | 4 | |a Indomethacin - pharmacology | |
| 650 | 4 | |a Pyrazoles - pharmacology | |
| 650 | 4 | |a Gene Expression Regulation - drug effects | |
| 650 | 4 | |a Oxidoreductases - metabolism | |
| 650 | 4 | |a Oxidative Stress - drug effects | |
| 650 | 4 | |a Reperfusion Injury - blood | |
| 650 | 4 | |a Malondialdehyde - blood | |
| 650 | 4 | |a Cyclooxygenase 2 Inhibitors - pharmacology | |
| 650 | 4 | |a Tumor Necrosis Factor-alpha - metabolism | |
| 650 | 4 | |a Nitric Oxide Synthase Type III - metabolism | |
| 650 | 4 | |a Liver - pathology | |
| 650 | 4 | |a Reperfusion Injury - pathology | |
| 700 | 1 | |a Ibrahim, Mohamed A |4 oth | |
| 700 | 1 | |a Amin, Entesar F |4 oth | |
| 700 | 1 | |a Ibrahim, Salwa A |4 oth | |
| 700 | 1 | |a Mohammed, Rehab K |4 oth | |
| 700 | 1 | |a Abdelrahman, Aly M |4 oth | |
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| 773 | 1 | 8 | |g volume:134 |g year:2015 |g pages:42-48 |
| 856 | 4 | 1 | |u http://dx.doi.org/10.1016/j.lfs.2015.04.025 |3 Volltext |
| 856 | 4 | 2 | |u http://www.ncbi.nlm.nih.gov/pubmed/26006041 |
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