Effects of Polygonum Multiflorum Thunb Extract on BDNF/TrkB and Its Downstream Signaling Pathways in Rat Model of Attention Deficit Hyperactivity Disorder
Objective To observe the effect of Polygonum Multiflorum Thunb extract(PME)on attention deficit hyperactivity disorder(ADHD)model rats and the related mechanism.Methods Spontaneously hypertension rat(SHR)were used as ADHD model.SHR rats were randomly divided into model group,tomoxetine treated group(4.5 mg/kg),PME low-(0.54 g/kg),medium-(1.08 g/kg),and high-(2.16 g/kg)dose group,Wistar-Kyoto(WKY)rats were selected as normal control group(n=10).Drugs were given twice a day for 4 weeks.After 4 weeks of intervention,docosahexaenoic acid(DHA)contents in prefrontal cortex were determined by ELISA kits.Western blot and RT-qPCR were used to detect associated factors in brain-derived neurotrophic factor(BDNF)/tyrosine kinase receptor B(TrkB)and its downstream signaling pathway,such as Gr62 and Ras3.Results Both tomoxetine and PME could ameliorate the spontaneous and impulsive behaviors of SHR rats.Compared with the normal group,the model group shared decreased DHA levels(P＜0.05),the mRNA and protein expressions of BDNF,TrkB,Grb2,Ras3 were significantly down-regulated(P＜0.01)in the prefrontal cortex,the expressions of protein of BDNF,TrkB,Grb2,Ras3 and the mRNA of BDNF、Ras3 were significantly down-regulated(P＜0.05)in the hippocampus.After 4 weeks of intervention,in the prefrontal cortex,the DHA levels and the mRNA expressions of BDNF,TrkB,Grb2,Ras3 in PME low、medium and high-dose groups were significantly up-regulated(P＜0.01),the expressions of protein of BDNF、TrkB、Grb2 in PME low,medium-dose groups and the expressions of protein of BDNF,Grb2,and Ras3 in PME high-dose group were significantly up-regulated(P＜0.05).In the hippocampus,the mRNA and protein expressions of BDNF,TrkB,Grb2,and Ras3 in PME high-dose group were significantly up-regulated(P＜0.05).Conclusion PME may have a role in improving the spontaneous and impulsive behaviors in SHR,which may be contributed to the regulation of BDNF/TrkB mediated downstream signaling pathways.
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