Abstract
We have shown that administration of Cinnamophilin (CINN) effectively reduced oxidative damage, DNA lipid peroxidation, neutrophil infiltration, and ischemic brain damage by inhibiting oxidative stress and the resulting inflammation in experimental stroke. In this study the potential CINN to ameliorate neutrophilic respiratory burst and reduce neutrophil infiltration was investigated. Neutrophils pretreated or co-treated with CINN, were stimulated by phorbol 12-myristate 13-acetate (PMA) and the levels of superoxide radical (O2-.) and hydrogen peroxide (H2O2) produced were determined by dihydroethidium (DHE) and dihydrorhodamine-123 (DHR) fluorescence assays, respectively, while myeloperoxidase activity (MPO) was measured by the guaiacol method. Our results showed that both pretreatment and co-treatment with CINN significantly inhibited H2O2 production in PMA-stimulated neutrophils. Additionally, cotreatment, but not pretreatment, with CINN effectively inhibited O2-. production in the PMA-stimulated neutrophils. Both treatments did not effectively reduce the MPO activity in neutrophil. Finally, animals treated with CINN at reperfusion brain insults significantly reduced brain infarction and neutrophil infiltration, as well as improved neurobehavioral outcome following cerebral ischemic reperfusion. These results support pluripotent neuroprotection actions offered by CINN against cerebral ischemia-reperfusion.
Highlights
Up to 40% of stroke patients did not recover their independence [1], which makes stroke a major public issue in the world
Following cerebral ischemia-reperfusion, neutrophils produce a variety of reactive oxygen species (ROS) when they are activated during inflammatory responses [12], a process which is known as the neutrophilic respiratory burst
Our results demonstrated that CINN could directly inhibit O2-. and H2O2 produced by the phorbol 12-myristate 13-acetate (PMA)-induced respiratory burst in neutrophils
Summary
Up to 40% of stroke patients did not recover their independence [1], which makes stroke a major public issue in the world. It is well known that neutrophils play an important role in the pathogenesis of ischemia reperfusion injury by releasing a variety of oxygen radicals including O2-., H2O2, and OH‐. Following cerebral ischemia-reperfusion, neutrophils produce a variety of reactive oxygen species (ROS) when they are activated during inflammatory responses [12], a process which is known as the neutrophilic respiratory burst. H2O2, which play an important mechanism of cerebral ischemia-reperfusion injury. It has been shown that neutrophil depletion or inhibition of neutrophil function exerted significant protective effects in ischemia reperfusioninduced brain injury [16-19]. One strategy to protect the brain against ischemic-reperfusion injury is to improve the endogenous antioxidant defense of the tissues at risk, to decrease oxidative damage by scavenging toxic free radicals [20-22] and to inhibit neutrophilic respiratory burst in activated neutrophils [23].
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