Effect of tiron on remote organ injury in rats with severe acute pancreatitis induced by L-arginine.
Acute pancreatitis (AP) is an acute inflammatory disorder of the pancreas that can be complicated by involvement of other remote organs. Oxidative stress is known to have a crucial role in the development of pancreatic acinar damage and one of the main causes in multisystem organ failure in experimental AP. The aim of the study was to determine the effect of tiron on pancreas and remote organ damage in L-arginine (L-Arg) induced AP rat model. Thirty-two male rats were divided in random into four groups: control, tiron, L-Arg, and tiron with L-Arg. At the end of the experiment, blood samples were withdrawn for biochemical analysis. The pancreas, lung, kidney, and liver were collected for histopathological examination. Estimation of pancreatic water content was done. Analysis of pulmonary, hepatic, renal, and pancreatic lipid peroxide levels (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) were carried out. Finally, nuclear factor kappa B (NF-κB) and transforming growth factor β1 (TGF-β1) expression in pancreatic tissue was determined. Results indicated that treatment with tiron significantly decreased lipid peroxide levels and markedly increased both SOD activity and GSH level. Moreover, histopathological analysis further confirmed that administration of tiron relatively ameliorates pancreatic acinar cells and remote organ damage. Increased immunoreactivity of NF-κB and TGF-β1 were reduced also by tiron treatment. These findings pointed out the protective role of the mitochondrial antioxidant, tiron against AP induced by L-Arg.
College of Pharmacy, Taibah University, El-Madinah, El-Munawarah, Saudi Arabia. hayamatya@hotmail.com.|Department of Clinical Pharmacology, Faculty of Medicine, Cairo University, Giza, Egypt. hayamatya@hotmail.com.
Hayam
H
Ateyya
Medical Laboratories Technology Department, Faculty of Applied Medical Sciences, Taibah University, El-Madinah El-Munawarah, Saudi Arabia.|Pathology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Heba M
HM
Wagih
College of Pharmacy, Taibah University, El-Madinah, El-Munawarah, Saudi Arabia.|Department of Clinical Pharmacology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Nagla A
NA
El-Sherbeeny
D014013:1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt / Q000494:pharmacology*; D000208:Acute Disease; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001120:Arginine; D015415:Biomarkers / Q000378:metabolism; D019610:Cytoprotection; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009102:Multiple Organ Failure / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013482:Superoxide Dismutase / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
D000975:Antioxidants; D015415:Biomarkers; D016328:NF-kappa B; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D009569:Nitric Oxide; D014013:1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt; D008315:Malondialdehyde; D001120:Arginine; D013482:Superoxide Dismutase; D005978:Glutathione
Acute pancreatitis; L-Arginine; NF-κB; Oxidative stress; TGF-β1; Tiron