Apocynin protects against global cerebral ischemia–reperfusion-induced oxidative stress and injury in the gerbil hippocampus

Content Provider	Semantic Scholar
Author	Wang, Qun Tompkins, Kenneth Simonyi, Agnès Korthuis, Ronald J. Sun, Grace Y.
Copyright Year	2006
Abstract	Increased production of reactive oxygen species (ROS) following cerebral ischemia-reperfusion (I/R) is an important underlying cause for neuronal injury leading to delayed neuronal death (DND). In this study, apocynin, a specific inhibitor for NADPH oxidase, was used to test whether suppression of ROS by the NADPH oxidase inhibitor can protect against ischemia-induced ROS generation and decrease DND. Global cerebral ischemia was induced in gerbils by a 5-min occlusion of bilateral common carotid arteries (CCA). Using measurement of 4-hydroxy-2-nonenal (HNE) as a marker for lipid peroxidation, apocynin (5 mg/kg body weight) injected i.p. 30 min prior to ischemia significantly attenuated the early increase in HNE in hippocampus measured at 3 h after I/R. Apocynin also protected against I/R-induced neuronal degeneration and DND, oxidative DNA damage, and glial cell activation. Taken together, the neuroprotective effects of apocynin against ROS production during early phase of I/R and subsequent I/R-induced neuronal damage provide strong evidence that inhibition of NADPH oxidase could be a promising therapeutic mechanism to protect against stroke damage in the brain.
Starting Page	182
Ending Page	189
Page Count	8
File Format	PDF HTM / HTML
DOI	10.1016/j.brainres.2006.03.060
PubMed reference number	16650838
Journal	Medline
Volume Number	1090
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/S0006899306007554
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/S0006899306007554?dgcid=api_sd_search-api-endpoint
Alternate Webpage(s)	https://doi.org/10.1016/j.brainres.2006.03.060
Journal	Brain Research
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article