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NEUROLOGY 1996;46:1437
© 1996 American Academy of Neurology

Synthetic peptide derived from the Bordetella pertussis bacterium reduces infarct volume after transient middle cerebral artery occlusion in the rat

R. L. Zhang, MD, M. Chopp, PhD, W. X. Tang, MD, Z. G. Zhang, MD, S. D. Putney, PhD and R. M. Starzyk, PhD

Department of Neurology, Henry Ford Health Sciences Center, Detroit, MI (Dr. Zhang) (Dr. Chopp) (Dr. Tang) (Dr. Zhang)
Department of Physics, Oakland University, Rochester, MI (Dr. Chopp) (Dr. Zhang)
Alkermes, Inc., Cambridge, MA. (Dr. Putney) (Dr. Starzyk)

Address correspondence and reprint requests to Dr. Michael Chopp, Henry Ford Hospital, Department of Neurology, 2799 West Grand Blvd., Detroit, MI 48202.

We explored the therapeutic potential of a peptide (F20) derived from the filamentous hemagglutinin of Bordetella pertussis in a model of ischemic cell injury after transient (2 hours) middle cerebral artery (MCA) occlusion in the rat. Animals were divided into two groups-(1) F20 peptide group: rats (n = 11) were subjected to 2 hours of transient MCA occlusion, and F20 peptide was administered intravenously (50 nmol) at 0 hours of reperfusion and intraperitoneally (150 nmol/dose) at 2, 4, 6, 8, 22, and 30 hours of reperfusion; (2) control group: rats (n = 10) were administered peptide F23 (a scrambled version of peptide F20) with the same experimental protocol as the F20 peptide group. Forty-six hours after reperfusion, animals were sacrificed, and brain tissue was stained with triphenyltetrazolium chloride for evaluation of tissue damage. To measure neutrophil numbers in ischemic tissue, myeloperoxidase (MPO) immunostaining was performed on a coronal cerebral section in each animal. There was a significant reduction of ischemic infarct volume (36%, p <0.05) in the F20 group of animals compared with the F23 group. The area of the ischemic lesion was highly correlated with the numbers of the immunoreactive MPO cells (r = 0.78, p <0.001). The data demonstrate that the F20 peptide significantly reduces infarct volume and intraparenchymal neutrophil numbers after transient MCA occlusion.

Supported by NIH grants PO1 NS23393 and ROI NS34184.

Received June 2, 1995. Accepted in final form August 18, 1995.




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