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 of S-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.