The Effects of Free Oxygen Radical Scavenger and Platelet-Activating Factor Antagonist Agents in Experimental Acute Pancreatitis

Preventive effects of enoxaparin and hesperidin in cerulein-induced acute pancreatitis in rats

“…It reacts rapidly with the superoxide radical, forming the highly reactive peroxynitrite anion (33). The ROS in the pancreatic tissues were significantly higher in CRL-induced rats than in the control animals in our study, and our results conform to those previously reported in literature (4,8,24). This study demonstrates the powerful therapeutic potential of the concomitant use of 2 agents-HES (17)(18)(19) and ENX (12,13,15)-that are clinically applied for their anticoagulant or anti-inflammatory properties.…”

“…Previous studies have reported that sequential injections of CRL induce mild and reversible pancreatitis limited to the pancreas (11,23). This non-fatal experimental pancreatitis model is widely used in research of cellular biological events and to investigate the pathogenesis of pancreatitis (10,11,23,24). Our study demonstrates that CRL initiates the development of all major parameters of acute pancreatitis in rats, including tissue edema, amylase overproduction, inflammation, and oxidative stress (1,2,10,11).…”

“…Nicotinamide adenine dinucleotide phosphate (NADPH)-related oxidase systems in the neutrophil membrane are activated by cytokines to transform oxygen to toxic metabolites such as superoxide, peroxide, and hydroxyradicals. Unstable and highly reactive toxic metabolites of molecular oxygen cause extensive damage to tissue, resulting in lipid peroxidation and enzyme and protein denaturation (4,8,24,(28)(29)(30)(31)(32). Further, ROS act on the arachidonic acid system and increase thromboxane production, which impairs tissue perfusion.…”

“…A detailed description of this study's methodology was published in our previous study (24). CRL and 0.6 mL saline were injected at hourly intervals into the rats in Group 2 and in the Sham Group, respectively, for a total of 7 times per group.…”

Nelfinavir/ritonavir reduces acinar injury but not inflammation during mouse caerulein pancreatitis

“…THE MECHANISMS LEADING TO cell death in acute pancreatitis are controversial (15,17), and theories include abnormal vesicular trafficking leading to activation of zymogens (39), toxic effects of intracellular calcium (17,27), and fatty acid ethyl esters (14), as well as activation of transcription factors (4), inflammatory mediators (6,36,50), cytoskeletal rearrangement (45), production of reactive oxygen species (5,42), and mitochondrial damage (9,11,12). During experimental mouse pancreatitis, both necrosis and apoptosis occur (3,10,12,13), although their roles during pancreatitis are controversial.…”