Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischemia-reperfusion injury in rats

  1. Pei-Lei Zhang MD,
  2. Hai-Tao Lu MD*,
  3. Jun-Gong Zhao MD*,
  4. Ming-Hua Li MD

DOI: 10.1111/j.1601-5215.2012.00649.x

Additional Information

Author Information

  1. Department of Diagnostic and Interventinal Radiololgy, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University, 600 Yi Shan Rd, Shanghai, 200233, People's Republic of China

*Hai-Tao Lu, and Jun-Gong Zhao E-mail: luhaitao1975@hotmail.com or zhaojungong11@yahoo.cn Fax: +86-21-64844183 Telephone: +86-21-64369181 Ext 8016

Publication History

  1. Accepted manuscript online: 11 JAN 2012 11:16AM EST

SEARCH

SEARCH BY CITATION

ARTICLE TOOLS

Get PDF (511K)

Keywords:

  • cerebral ischemia;
  • dl-3n-butylphthalide;
  • vascular endothelial growth factor;
  • reperfusion injury;
  • rats;
  • neuroprotection

Objective: To investigate the effect of dl-3n-butylphthalide (NBP) on the protection of cerebral tissue and possible mechanism on ischemia reperfusion injury, and to ask whether NBP therapy can extend the reperfusion window in an experimental stroke model in rats.

Methods: Seventy-two Sprague-Dawley (SD) rats were randomly divided into sham operation, ischemia-reperfusion, and ischemia-reperfusion with NBP groups. Focal cerebral ischemia was induced using the modified intraluminal thread method and maintained for 2, 3, or 4 hours. The ischemia-reperfusion group received reperfusion immediately after ischemia-reperfusion. The NBP group received intraperitoneal injection of NBP immediately after ischemia, followed by reperfusion. The sham operation group received only injection of physiological saline. The cerebral infarction volume and neurological deficit were analyzed, and Vascular endothelial growth factor (VEGF) expression in brain tissues was visualized by immunohistochemistry.

Results: NBP treatment caused a significant decrease in both infarction volume and neurological deficit compared with the ischemia-reperfusion group at corresponding time points in each (P<0.05). In the NBP group the infarction volume and neurological deficit did not change with different ischemia times. The expression of VEGF was significantly decreased in the ischemia-reperfusion group compared with the sham group (P <0.01), while this change was partly prevented in the NBP group (P<0.01). The expression of VEGF in brain tissue in both the NBP and ischemia-reperfusion groups gradually decreased when the ischemic period was prolonged.

Conclusion: NBP treatment has a protective effect against cerebral ischemia, which possible mechanism maybe related to the VEGF expression, and may extend the reperfusion window for subsequent salvage of cerebral ischemia by reperfusion.

Get PDF (511K)