Many complicated mechanisms are involved in brain ischemia and the role of inflammatory factors in the progression of post-ischemic injury is inevitable. In present study, anti-inflammatory effect of berberine has been investigated in reperfusion injury after acute ischemic stroke. Male Wistar rats weighing 250-270 gr were randomly divided into four cohorts: healthy rats (control, n=20), sham-o...

Over the past two decades, the mortality from acute myocardial infarction (AMI) has been reduced dramatically. Timely reperfusion is the most powerful intervention for limiting infarct size, alongside antiplatelet, antithrombotic and anti-ischemic therapies. Paradoxically, reperfusion itself can also exacerbate myocardial injury, so called ‘‘reperfusion injury’’, which can cause additional card...

OBJECTIVE Endothelial dysfunction by the loss of nitric oxide (NO) is a critical event during reperfusion of ischemic myocardium. Reduced NO availability signals important pathophysiological changes leading to myocardial reperfusion injury. We have recently shown that NO biosynthesis can be disturbed by the endogenous NO synthase (NOS) inhibitor ADMA and that these changes are mediated by an im...

The cardiac ATP-sensitive potassium (KATP) channel is thought to be a complex composed of an inward rectifier potassium channel (Kir6.1 and/or Kir6.2) subunit and the sulfonylurea receptor (SUR2). This channel is activated during myocardial ischemia and protects the heart from ischemic injury. We examined the transcriptional expression of these genes in rats with myocardial ischemia. 60 min of ...

BACKGROUND Myocardial apoptosis is heavily implicated in the myocardial damage caused by ischemia-reperfusion (I/R). Toll-like receptor 4 (TLR4) is a potent inducer of these apoptotic cascades. In contrast, the radioprotective 105 kDa protein (RP105) is a specific negative regulator of TLR4 signaling pathways. However, the precise mechanisms by which RP105 inhibits myocardium apoptosis via TLR4...

Despite early recanalization of an occluded infarct artery, tissue reperfusion remains impaired in more than one-third of the acute myocardial infarction (AMI) patients owing to a process of reperfusion injury. The role of systemic inflammation in triggering this phenomenon is unknown. Proinflammatory factors (hs-CRP, TNF-alpha ) and anti-inflammatory mediators (IL-1 receptor antagonist, IL-10)...

BACKGROUND Ulinastatin has anti-inflammatory properties and protects organs from ischemia/reperfusion-induced injury. The aim of this study was to investigate whether ulinastatin provides a protective effect on a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model and to determine whether the anti-inflammatory response is related to its myocardial protective effect. ...

In the setting of acute myocardial infarction, reperfusion of ischemic myocardium carried out early after coronary occlusion can salvage reversibly injured, viable myocardium. Although still controversial, however, reperfusion itself may cause a population of reversibly injured cells to die, a phenomenon termed lethal reperfusion injury.1 A variety of pharmacological agents have been studied to...

Abstract Coronary heart disease leading to myocardial ischemia is a major cause of failure. A hallmark failure fibrosis. Using murine model ischemia/reperfusion injury (IRI), we showed that, following IRI, in mice genetically deficient the central factor complement system, C3, necrosis was reduced compared with WT mice. Four weeks after ischemic period, C3 −/−mice had significantly less cardiac...

The damage inflicted on the myocardium during acute myocardial infarction is the result of 2 processes: ischemia and subsequent reperfusion (ischemia/reperfusion injury). During the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have been widely incorporated into clinical practice. The remarkable reduction in death rates achieved with these therapies has res...