作者: Seham A. Abdel-Gaber , Mohamed A. Ibrahim , Entesar F. Amin , Salwa A. Ibrahim , Rehab K. Mohammed
DOI: 10.1016/J.LFS.2015.04.025
关键词: Liver injury 、 Nitric oxide 、 Malondialdehyde 、 Cyclooxygenase 、 Enos 、 Glutathione peroxidase 、 Pharmacology 、 Superoxide dismutase 、 Anesthesia 、 Oxidative stress 、 Medicine
摘要: Abstract Aim Ischemia–reperfusion (IR) injury represents an important pathological process of liver during major hepatic surgery. The role cyclooxygenase (COX) enzymes in the pathogenesis ischemia–reperfusion (IR)-induced is not clear. This study investigated effect a selective COX-2 inhibitor, celecoxib, versus non-selective, indomethacin, on IR rats. Materials and methods Hepatic was induced adult male animals were divided into 4 groups: normal control (sham group), non-treated group; IR-indomethacin-treated IR-celecoxib-treated group. Liver evaluated by serum alanine aminotransferase (ALT) histopathological examination tissues. tissue content oxidative stress parameters glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase, malondialdehyde (MDA), nitric oxide (NO) inflammatory marker, tumor necrosis factor-alpha, (TNF-α) measured. Moreover, immunohistochemical detection endothelial NO synthase (eNOS), inducible (iNOS), caspase-3 performed. Key findings Celecoxib, but significantly attenuated as evidenced reduction ALT well improvement scoring. Such associated with attenuation TNF-α, along modulation expression eNOS, iNOS tissue. Significance present concluded that inhibition (but non-selective), hepatoprotective against injury; indicating differential COX-1 COX-2. Modulation iNOS, eNOS might participate protective COX-2-inhibitors.