Effect of selective versus non-selective cyclooxygenase inhibitors on ischemia-reperfusion-induced hepatic injury in rats
Copyright © 2015 Elsevier Inc. All rights reserved..
AIM: 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.
MATERIALS AND METHODS: 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.
KEY FINDINGS: 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.
SIGNIFICANCE: 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: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2015 |
|---|---|
| Erschienen: |
2015 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:134 |
|---|---|
| Enthalten in: |
Life sciences - 134(2015) vom: 01. Aug., Seite 42-8 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Abdel-Gaber, Seham A [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 16.09.2015 Date Revised 19.11.2015 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.lfs.2015.04.025 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM249320894 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM249320894 | ||
| 003 | DE-627 | ||
| 005 | 20231224153327.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231224s2015 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.lfs.2015.04.025 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0831.xml |
| 035 | |a (DE-627)NLM249320894 | ||
| 035 | |a (NLM)26006041 | ||
| 035 | |a (PII)S0024-3205(15)00278-7 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 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 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 16.09.2015 | ||
| 500 | |a Date Revised 19.11.2015 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2015 Elsevier Inc. All rights reserved. | ||
| 520 | |a AIM: 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 | ||
| 520 | |a MATERIALS AND METHODS: 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 | ||
| 520 | |a KEY FINDINGS: 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 | ||
| 520 | |a SIGNIFICANCE: 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 | ||
| 650 | 4 | |a Comparative Study | |
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Celecoxib-ischemia–reperfusion | |
| 650 | 4 | |a Cyclooxygenase inhibitors | |
| 650 | 4 | |a Hepatic ischemia–reperfusion | |
| 650 | 4 | |a Indomethacin-ischemia–reperfusion | |
| 650 | 7 | |a Cyclooxygenase 2 Inhibitors |2 NLM | |
| 650 | 7 | |a Pyrazoles |2 NLM | |
| 650 | 7 | |a Sulfonamides |2 NLM | |
| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a Malondialdehyde |2 NLM | |
| 650 | 7 | |a 4Y8F71G49Q |2 NLM | |
| 650 | 7 | |a Oxidoreductases |2 NLM | |
| 650 | 7 | |a EC 1.- |2 NLM | |
| 650 | 7 | |a Nitric Oxide Synthase Type II |2 NLM | |
| 650 | 7 | |a EC 1.14.13.39 |2 NLM | |
| 650 | 7 | |a Nitric Oxide Synthase Type III |2 NLM | |
| 650 | 7 | |a EC 1.14.13.39 |2 NLM | |
| 650 | 7 | |a Nos2 protein, rat |2 NLM | |
| 650 | 7 | |a EC 1.14.13.39 |2 NLM | |
| 650 | 7 | |a Nos3 protein, rat |2 NLM | |
| 650 | 7 | |a EC 1.14.13.39 |2 NLM | |
| 650 | 7 | |a Alanine Transaminase |2 NLM | |
| 650 | 7 | |a EC 2.6.1.2 |2 NLM | |
| 650 | 7 | |a Casp3 protein, rat |2 NLM | |
| 650 | 7 | |a EC 3.4.22.- |2 NLM | |
| 650 | 7 | |a Caspase 3 |2 NLM | |
| 650 | 7 | |a EC 3.4.22.- |2 NLM | |
| 650 | 7 | |a Celecoxib |2 NLM | |
| 650 | 7 | |a JCX84Q7J1L |2 NLM | |
| 650 | 7 | |a Indomethacin |2 NLM | |
| 650 | 7 | |a XXE1CET956 |2 NLM | |
| 700 | 1 | |a Ibrahim, Mohamed A |e verfasserin |4 aut | |
| 700 | 1 | |a Amin, Entesar F |e verfasserin |4 aut | |
| 700 | 1 | |a Ibrahim, Salwa A |e verfasserin |4 aut | |
| 700 | 1 | |a Mohammed, Rehab K |e verfasserin |4 aut | |
| 700 | 1 | |a Abdelrahman, Aly M |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Life sciences |d 1965 |g 134(2015) vom: 01. Aug., Seite 42-8 |w (DE-627)NLM000007579 |x 1879-0631 |7 nnns |
| 773 | 1 | 8 | |g volume:134 |g year:2015 |g day:01 |g month:08 |g pages:42-8 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.lfs.2015.04.025 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 134 |j 2015 |b 01 |c 08 |h 42-8 | ||