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Mechanism of neuroprotective effects of fibroblast growth factor 2 in the mouse model of ALS
Author(s): Zhang Rui, Zang Dawei
Pages: 886-
890
Year: 2016
Issue:
11
Journal: National Medical Journal of China
Keyword: FGF-2; Amyotrophic Lateral Sclerosis; SOD1; Neural Precursor Cell; S-IR bouton;
Abstract: Objective To examine the neuroprotective effects of FGF-2 and explore the underlying mechanisms involved in its effects on neural precursor cells (NPCs) and S-IR boutons.Methods The mice models were established,and the animals were randomly divided into 3 groups:non-transgenic wild type group (WT),superoxide dismutase (SOD)1 G93A G1H transgenic group (SOD1),and fibroblast growth factor (FGF)-2-treated group (FGF-2),each group 40 mice.Mice of FGF-2 group were treated with FGF-2 at postnatal day 60 (P60).These three groups were examined at postnatal day 90 (P90) and 120 (P120).The changes of NPCs and S-IR boutons were checked by means of immunohistochemical detection.Results When mice were examined at P90 and P120,the number of Nestin + NPCs was (47 ± 24) and (147 ± 45) in the SOD1 group,(77 ±27) and (285 ± 103) in the FGF-2 group.A marked increase was detected in the FGF-2 mice compared to the SOD1 mice at P120 (P < 0.01).At P120 there was a clear decrease in the density ofS-IR boutons in the SOD1 (0.5 ±0.1) and FGF-2 (0.8 ±0.1) mice compared to the WT (0.9 ±0.1) mice,but a more significant decrease in the density of S-IR boutons was detected in the SOD1 mice compared to the FGF-2 mice (P < 0.05).Conclusion FGF-2 may be a useful treatment to provide neuroprotection against neurodegeneration in amyotrophic lateral sclerosis (ALS) by encouraging the proliferation of NPCs and delaying the decrease in the density of S-IR boutons.
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