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• Ding, Z
• Wu, B
• Zhang, W
• Lu, X
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• Miao, Y
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• Zhang, W
• Lu, X
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Int. J. Mol. Sci. 2012, 13(5), 6089-6101; doi:10.3390/ijms13056089

Article

Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the Same Effect on Inhibition of Apoptosis

Zhe-Min Ding ¹ , Bing Wu ² , Wei-Qiao Zhang ³ , Xiao-Jie Lu ¹ , Yu-Chang Lin ¹ , Yong-Jian Geng ⁴  and Yi-Feng Miao ^1,*

¹ Neuroscience Center, Wuxi No. 2 Hospital, Nanjing Medical University, Wuxi 214002, China ² Department of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China ³ Department of Neurosurgery, Yuyao People’s Hospital, Yuyao 315472, China ⁴ University of Texas Medical School at Houston, Houston, TX 77030, USA

* Author to whom correspondence should be addressed.

Received: 27 March 2012; in revised form: 3 May 2012 / Accepted: 14 May 2012 / Published: 18 May 2012

Download PDF Full-Text [399 KB, uploaded 18 May 2012 12:06 CEST]

Abstract: Transient forebrain or global ischemia induces neuronal death in vulnerable CA1 pyramidal cells with many features. A brief period of ischemia, i.e., ischemic preconditioning, or a modified reperfusion such as ischemic postconditioning, can afford robust protection of CA1 neurons against ischemic challenge. Therefore, we investigated the effect of ischemic preconditioning and postconditioning on neural cell apoptosis in rats. The result showed that both ischemic preconditioning and postconditioning may attenuate the neural cell death and DNA fragment in the hippocampal CA1 region. Further western blot study suggested that ischemic preconditioning and postconditioning down-regulates the protein of cleaved caspase-3, caspase-6, caspase-9 and Bax, but up-regulates the protein Bcl-2. These findings suggest that ischemic preconditioning and postconditioning have a neuroprotective role on global brain ischemia in rats through the same effect on inhibition of apoptosis.

Keywords: brain ischemic injury; ischemic preconditioning; ischemic postconditioning; apoptosis; neuroprotection

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