title: Self-assembling peptide nanofiber scaffold promotes the reconstruction of acutely injured brain.
abstract: Traumatic brain injury (TBI) or brain surgery may cause extensive loss of cerebral parenchyma. However, no strategy for reconstruction has been clinically effective. Our previous study had shown that self-assembling peptide nanofiber scaffold (SAPNS) can bridge the injured spinal cord, elicit axon regeneration, and eventually promote locomotor functional recovery. In the present study we investigated the effect of SAPNS for the reconstruction of acutely injured brain. The lesion cavity of the injured cortex was filled with SAPNS or saline immediately after surgically induced TBI, and the rats were killed 2 days, 2 weeks, or 6 weeks after the surgery for histology, immunohistochemistry, and TUNEL studies. Saline treatment in the control animals resulted in a large cavity in the injured brain, whereas no cavity of any significant size was found in the SAPNS-treated animals. Around the lesion site in control animals were many macrophages (ED1 positive) but few TUNEL-positive cells, indicating that the TBI caused secondary tissue loss mainly by means of necrosis, not apoptosis. In the SAPNS-treated animals the graft of SAPNS integrated well with the host tissue with no obvious gaps. Moreover, there were fewer astrocytes (GFAP positive) and macrophages (ED1 positive) around the lesion site in the SAPNS-treated animals than were found in the controls. Thus, SAPNS may help to reconstruct the acutely injured brain and reduce the glial reaction and inflammation in the surrounding brain tissue.
  
  
  BACKGROUND
  Self-assembling peptide nanofiber scaffold (SAPNS) was reported earlier to bridge the injured spinal cord, elicit axon regeneration, and promote locomotor recovery. In this study the effect of SAPNS for the reconstruction of acutely injured brain was investigated. In SAPNS-treated animals the graft integrated well with the host tissue with no obvious gaps. SAPNS may help to reconstruct the acutely injured brain and reduced the glial reaction and inflammation in the surrounding brain tissue.
authors.affiliation: Department of Anatomy, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
authors.forename: Jiasong
authors.initials: J
authors.lastname: Guo
authors.forename: Ka Kit Gilberto
authors.initials: KK
authors.lastname: Leung
authors.forename: Huanxing
authors.initials: H
authors.lastname: Su
authors.forename: Qiuju
authors.initials: Q
authors.lastname: Yuan
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.forename: Tak-Ho
authors.initials: TH
authors.lastname: Chu
authors.forename: Wenming
authors.initials: W
authors.lastname: Zhang
authors.forename: Jenny Kan Suen
authors.initials: JK
authors.lastname: Pu
authors.forename: Gloria Kowk Po
authors.initials: GK
authors.lastname: Ng
authors.forename: Wai Man
authors.initials: WM
authors.lastname: Wong
authors.forename: Xiang
authors.initials: X
authors.lastname: Dai
authors.forename: Wutian
authors.initials: W
authors.lastname: Wu
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology* / Q000601:surgery; D001930:Brain Injuries / Q000188:drug therapy / Q000473:pathology / Q000601:surgery / Q000628:therapy*; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D005260:Female; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology; D049329:Nanostructures / Q000737:chemistry*; D009457:Neuroglia / Q000187:drug effects / Q000276:immunology; D010455:Peptides / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000187:drug effects*; D054457:Tissue Scaffolds / Q000737:chemistry*
chemical_list: D010455:Peptides