[Effect of willed movement therapy on GFAP and SYP expression in rats with cerebral ischemia-reperfusion]

Nan Fang Yi Ke Da Xue Xue Bao. 2011 Sep;31(9):1543-6.
[Article in Chinese]

Abstract

Objective: To determine the effect of willed movement on the expression of glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) in adult rats with cerebral ischemia-reperfusion, and explore the mechanism of willed movement in promoting nerve repair and regeneration.

Methods: Adult rat models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion (MCAO) for 2 h followed by a 24-h reperfusion. The models were then divided randomly into 3 groups, namely the model group, environmental modification (EM) group, and willed movement (WM) group. In each group, neurological deficits were evaluated at 3, 7 and 15 days after reperfusion. Immunohistochemistry and immunofluorescence assay were employed to examine the expression of GFAP and SYP in the brain tissue near the ischemic foci.

Results: The rats in WM group showed lessened neurological deficits at 15 days and lowered expression of GFAP and SYP at 7 and 15 days after reperfusion compared with the model and EM groups (P<0.05). No significant difference was found in the expression of GFAP or SYP between the model group and EM group at any time points.

Conclusion: Willed movement can promote the functional recovery of neurological deficits following cerebral ischemia-reperfusion probably in relation to enhanced GFAP and SYP expressions in the ischemic brain tissues.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Ischemia / metabolism*
  • Brain Ischemia / therapy
  • Disease Models, Animal
  • Exercise Therapy / methods*
  • Glial Fibrillary Acidic Protein / metabolism*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / therapy*
  • Synaptophysin / metabolism*

Substances

  • Glial Fibrillary Acidic Protein
  • Synaptophysin
  • Syp protein, rat