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(Stroke. 2008;39:2362.)
© 2008 American Heart Association, Inc.

Original Contributions

Ischemic Postconditioning Inhibits Apoptosis After Focal Cerebral Ischemia/Reperfusion Injury in the Rat

Bianzhi Xing, MD; Hui Chen, MD; Min Zhang, PhD; Dongming Zhao, MD; Rui Jiang, MD; Xiuheng Liu, PhD Suming Zhang, PhD

From the Department of Neurology (B.X., M.Z., S.Z.), Department of Orthopaedics (D.Z.), and Department of Oncology (R.J.), Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, and the Department of Urology (H.C., X.L.), Renmin Hospital of Wuhan University, Wuhan, China.

Correspondence to Suming Zhang, PhD, and Min Zhang, PhD, Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hang Kong Road 13, Wuhan, 430030, China. E-mail drzhangsuming{at}163.com

Background and Purpose— Ischemic postconditioning (Postcond) is defined as a series of intermittent interruptions of blood flow in the early phase of reperfusion that mechanically alters the hydrodynamics of reperfusion. A recent study showed that Postcond reduced infarct size in cerebral ischemia/reperfusion (I/R) injury. However, little is known about the mechanisms of Postcond in cerebral I/R injury. In the present study, we investigated the effects of Postcond in focal cerebral I/R injury in the rat middle cerebral artery occlusion model.

Methods— Adult male Sprague-Dawley rats were treated with Postcond after 60 minutes of occlusion (beginning of reperfusion). Neurologic scores and infarct volumes were assessed at 24 and 72 hours. Oxidative stress was evaluated by malondialdehyde assay, and apoptosis-related molecules were studied by Western blotting.

Results— Postcond treatment upregulated Bcl-2 and heat-shock protein 70 expression and downregulated cytochrome c release to the cytosol, Bax translocation to the mitochondria, and caspase-3 activity. Postcond treatment also reduced infarct volumes and oxidative stress levels and improved neurologic scores compared with the I/R-only group.

Conclusions— These findings indicate that Postcond inhibits focal cerebral I/R injury. This neuroprotective effect is likely achieved by antiapoptotic mechanisms.

Key Words: ischemic postconditioning • ischemia/reperfusion • apoptosis • middle cerebral artery occlusion model