Cardiac Reactive Oxygen Species After Traumatic Brain InjuryCardiovascular complications after traumatic brain injury (TBI) contribute to morbidity and mortality and may provide a target for therapy. We examined blood pressure and left ventricle contractility after TBI, and tested the hypothesis that β-adrenergic blockade would decrease oxidative stress after TBI.
Curcumin Protects Against Ischemia/Reperfusion Injury in Rat Skeletal MuscleCurcumin has been shown to decrease ischemia-reperfusion (I/R) injury in kidney or brain tissues. In this study, the effects of curcumin were evaluated in skeletal muscle during I/R injury.
Suppression of Experimental Abdominal Aortic Aneurysm in a Rat Model by the Phosphodiesterase 3 Inhibitor CilostazolThe present experiments sought to determine whether cilostazol, a selective inhibitor of cyclic adenosine monophosphate (cAMP) phosphodiesterase 3 (PDE3), suppressed elastase-induced abdominal aortic aneurysm (AAA) development in a rat model.
Triptolide Alleviates Hepatic Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and Inhibiting NF-κB Activity in MiceHepatic I/R injury is unavoidable in liver transplantation and surgery. This remains a significant problem in surgical procedures. The purpose of this study was to investigate the effects of triptolide on liver ischemia/reperfusion (I/R) injury and related mechanisms in mice.
β-Glucan Protects against Lung Injury Induced by Abdominal Aortic Ischemia-Reperfusion in RatsAortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute lung injury following abdominal aortic surgery. The aim of our study was to examine the effect of β-glucan on lung injury induced by abdominal aortic IR in rats.
Macrophage Migration Inhibitory Factor (MIF) and Manganese Superoxide Dismutase (MnSOD) as Early Predictors for Survival in Patients with Severe Sepsis or Septic ShockSevere sepsis, septic shock, and resulting organ failure appear as the most common cause of death in intensive care medicine. Inflammatory mediators (interleukin-6/IL-6), cell adhesion molecules (intercellular adhesion molecule-1/ICAM-1, vascular cell adhesion molecule-1/VCAM-1), and redox active substances (manganese superoxide dismutase/MnSOD, macrophage migration inhibitory factor/MIF) must be considered to be central hubs in the inflammatory process. However, their exact pathophysiologic function and prognostic value are still poorly understood.