http://www.sciencedirect.com/science/article/pii/S0304394015302573
Choose an option to locate/access this article:
Check if you have access through your login credentials or your institution
Check accessHighlights
- •
- A serum fraction (100K) was easily derived from serum.
- •
- 100K/bFGF enhanced cell proliferation at SVZ area and infarcted brain.
- •
- 100K/bFGF increased the number of MAP-2 cells at infarcted brain in MCAO rat.
- •
- 100K/bFGF improved animals' motor coordination of MCAO rat.
Abstract
Enhancing
endogenous neurogenesis is a potential therapeutic strategy in stroke
treatment. We have previously domonstrated that treatment with a
fraction of serum with molecular weight of less than 100kDa (100K)
combined with bFGF promoted neurogenesis of cultured stem and progenitor
cells (NSPCs). In this study, we further evaluated the efficacy of
intraventricular administration of 100K with bFGF (100K/bFGF) in a rat
model of transient middle cerebral artery occlusion (MCAO). Rats
administered 100K/bFGF on post-stroke day 1 exhibited a higher number of
Ki67 and Nestin immunoreactive cells at the subventricular zone (SVZ)
area and in the infarcted brain, indicating promotion of NSPCs
proliferation. The 100K/bFGF treatment also predominantly increased the
number of MAP-2 immunoreactive cells rather than GFAP immunoreactive
cells at the SVZ area and in the infarcted regions, implying that
100K/bFGF dominated NSPCs differentiating into neurons rather than
astrocytes. Importantly, treatment with 100K/bFGF significantly improved
the animals' motor coordination. These findings demonstrated that
treatment with a low serum fraction and bFGF benefited ischemic stroke
likely through promotion of the proliferation and neuronal
differentiation of endogenous NSPCs.
No comments:
Post a Comment