Cinnamophilin Inhibits Neutrophilic Respiratory Burst and Protects Against Ischemia-Reperfusion Brain DamageYu-Wen Lin1, Shih-Huang Tai1, Chih-Hao Tien1, Sheng-Yang Huang1, Che-Chao Chang1, Tian-Shung Wu2, Wei-Sheng Juan1, Hung-Yi Chen3 and E-Jian Lee1*
- *Corresponding Author:
- E-Jian Lee
Department of Surgery
National Cheng Kung University Medical Hospital
138 Sheng-Li Road, Tainan, Taiwan
Tel: +886-6-235-3535 ext.5186
E-mail: [email protected]
Received date: October 19, 2013; Accepted date: November 18, 2013; Published date: November 21, 2013
Citation: Lin YW, Tai SH, Tien CH, Huang SY, Chang CC, et al. (2013) Cinnamophilin Inhibits Neutrophilic Respiratory Burst and Protects Against Ischemia-Reperfusion Brain Damage. Pharmaceut Anal Acta 4:272. doi: 10.4172/2153-2435.1000272
Copyright: © 2013 Lin YW, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.