Effect and mechanism of adipose mesenchymal stem cell exosomes on memory impairment after brain trauma
Objective To investigate the effect and mechanism of adipose mesenchymal stem cell exosomes on memory impairment af-ter brain trauma.Methods Extraction of adipose mesenchymal stem cell exosomes by differential centrifugation.A total of 24 SD rats were randomly divided into control group,brain trauma group and exosome group,with 8 rats in each group.The rats in the control group were not treated,the brain trauma model of rats in the brain trauma group and exosome group was established by falling body impact method,and the exosome group was injected 300 μg of adipose mesenchymal stem cell exosomes intravenously after the model was established.After 7 days,the memory ability of rats was evaluated by water maze,and the damage and repair of brain tissue were evaluated by wet and dry weight,Tau and S100β proteins.The expressions of nerve growth factor(NGF)and brain-derived neuro-trophic factors(BDNF)in rat brain were detected by enzyme-linked immunosorbent assay.The expression of TrkA and TrkB in rat brain was detected by Western blot.Results The wet-dry ratio,Tau and S100β protein expression levels in brain trauma group were higher than those in control group,and the differences were statistically significant(P<0.05).The wet-dry ratio,Tau and S100β pro-tein expression levels in exosome group were lower than those in brain trauma group,and the differences were statistically significant(P<0.05).Compared with the brain trauma group,the escape latency of rats in the exosome group was significantly shortened from day 2 to 5,the frequency of crossing the platform was significantly increased,the target quadrant time was prolonged,the expression of NGF and BDNF in brain tissue was significantly increased,and the protein expressions of TrkA and TrkB were increased,with statisti-cal significance(P<0.05).Conclusion Adipose mesenchymal stem cell exosomes can alleviate post-traumatic memory impairment,and the mechanism is related to the regulation of neurotrophic factors and TrkA/TrkB receptors.
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万方数据
维普
