effect of melatonin on pentraxin-3 level and nuclear factor-kappa beta immunohistochemical expression on acetic acid-induced colitis and their relationship to pathophysiology of the disease

Taking into consideration the presence of melatonin [MEL] in gastrointestinal [GI] tissue and its role in gastrointestinal tract [GIT] physiology, it is practical to speculate that melatonin could influence inflammation-related GI disorders, including ulcerative colitis [UC]. We hypothesized the preventive, short and long term effects of melatonin administration on acetic acid [AA] induced colitis in rats and its potential underlying mechanism. We evaluate the immunohistochemical expression of nuclear factor NF-kappa beta [NF-kappa beta]. We also estimated the relation between AA-induced colitis and pentraxin-3 [PTX-3] serum level. The animals were divided into 5 groups. Control group, AA-induced-colitis group, Pre-treated group, Short-term treated group, and Long-term treated group. At the end of the experiment, blood samples were taken for measurement of PTX-3, lipid peroxide [LP] and total thiols [TT]. Colon was taken for histopathological examination and immunohistochemical study for detection of NF- kappa beta expression. MEL is effective in prevention and short-term treatment of AA-induced colitis as indicated by attenuating the colitis symptoms such as rectal bleeding, reduction of the body weight, the increase in the colonic weight and reduction of the severity of mucosal damage dramatically. MEL administration, also decreased NF- kappa beta immunohistochemical expression, decreased serum level of LP and PTX-3 and increased serum level of TT. However, in long-term treatment MEL has negative effect on AA-induced colitis. MEL is effective in prevention and short-term treatment of colonic inflammatory process while long-term treatment exacerbate the colitis. The outcome also indicated that melatonin contributes in a variety of guard mechanisms against colonic inflammatory processes by inhibiting the NF- kappa beta and conserving the vital endogenous antioxidant reserve of TT, thus dipping the level of colonic damage, mainly in the early phase of colitis

Effect of vagus nerve stimulation on serum level of pentraxin-3 at focal transient cerebral ischemia and reperfusion in adult male new zealand rabbits

Regarding that oxidative stress, distinguished by the overproduction of reactive oxygen species [ROS], has been implicated in the pathophysiology of cerebral ischemia. Pentraxin-3 [PTX-3] plays an important role in innate immune responses and in inflammatory disease. However, no study has evaluated PTX3 in animal models with cerebral ischemia and reperfusion. Aim of the work: is to assess the anti-inflammatory and anti-oxidant effect of vagus nerve stimulation [VNS] on focal model of transient cerebral ischemia and reperfusion. Focal transient cerebral I/R was induced by occlusion of right common carotid artery [CCA] for 30 minutes followed by reperfusion for one hour. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. VNS started 15 min after right CCA ligation and lasted 15 min after reperfusion and delivered for 30 s at every 5 min. All the procedures were duplicated but no stimulus was delivered in the control group. Serum level of pentraxin-3, lipid peroxide and total thiols were determined at baseline, at end of ischemia and at end of reperfusion and the animal decapitated and neuronal damage was evaluated. VNS causes reduction of the ischemic features with revival of the cell shape and size, increased serum levels of pentraxin-3 and total thiols whereas the level of lipid peroxide was diminished. The observed diversity in pentraxin-3, lipid peroxide and total thiols levels in cerebral I/R, which may reflect relative roles in the bioactivity of the animal. The anti-inflammatory and anti-oxidant role of vagus nerve stimulation in cerebral I/R in rabbits, may represent a marker of altered cerebral function, that provide potential therapeutic applications