Basic fibroblast growth factor improves learning and memory deficits in a mouse model of vascular dementia Associated with the role of free radicals clearance?

作者：Qu Xian^*; Li Chunying; Su Chang; Li Bing; Wang Liying

来源：Neural Regeneration Research, 2010, 5(13): 1015-1019.

DOI：10.3969/j.issn.1673-5374.2010.13.010

• basic fibroblast growth factor
• vascular dementia
• Morris water maze
• superoxide dismutase
• malondialdehyde
• neurodegenerative disease
• neural regeneration

BACKGROUND: Basic fibroblast growth factor (bFGF) exhibits neuroprotective functions, but the possible mechanisms of bFGF on vascular dementia remain unclear.
OBJECTIVE: To explore the neuroprotective effects of bFGF on a mouse model of vascular dementia, with focus on oxidative damage.
DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Medical College of Beihua University from March to December 2008.
MATERIALS: bFGF was purchased from Peprotech, USA.
METHODS: A total of 80 healthy, Kunming mice were randomly assigned to control, sham-surgery, model, and bFGF groups. The model and bFGF groups were used to establish vascular dementia models by repetitive cerebral ischemia-reperfusion in a conscious state. In addition, bFGF group mice were intraperitoneally injected with bFGF (100 mu g/kg) following model establishment, once a day for 7 consecutive days.
MAIN OUTCOME MEASURES: The Morris water maze was used to determine the influence of bFGF on learning and memory abilities in vascular dementia mice. The pathomorphological changes in hippocampal CA1 neurons were observed by Nissl staining. Superoxide dismutase and malondialdehyde changes were analyzed using biochemical analysis methods. Annexin V-FITC/PI-double-labeled flow cytometry was used to detect neuronal apoptosis.
RESULTS: Learning and memory functions in model mice significantly decreased, as characterized by prolonged latency and reduced time and number of platform crossings (P < 0.01, P < 0.05). Superoxide dismutase activity was significantly reduced, malondialdehyde content was significantly increased (P < 0.01), and hippocampal neuronal apoptosis was increased (P < 0.01) following vascular dementia. bFGF increased superoxide dismutase activity, decreased malondialdehyde content, and reduced hippocampal neuronal apoptosis (P < 0.01), which resulted in improved learning and memory in mice with vascular dementia.
CONCLUSION: bFGF improved learning and memory deficits in mice with vascular dementia by reducing free radical injury and inhibiting hippocampal neuronal apoptosis.

• 出版日期2010-7
• 单位北华大学