Study on the expression of BDNF in hippocampus and cerebrum in D-galactose-induced aging rats
Song Shi
Abstract
Song Shi
Abstract
Objective To explore the influence of Radix Polygoni Multiflori(RPM) on brain-derived neurotrophic factor(BDNF) expression of hippocampus and brain in the senile rat induced by D-galactose(D-gal).Methods 36 rats were randomly divided into control,senile model and RPM groups.The model and RPM group were injected with D-gal 0.125 g·kg-1·d-1 by subcutaneous injection continuously for 60 days,while control group were administered with the same dose of normal saline per day.The ability of learning and memory of rats were measured in Morris water maze,the amount of mRNA of BDNF was measured by RT-PCR and the amount of protein of BDNF was measured by Western blot.Results The escape latency of model group was longer than that of control group(P 0.05),and there was no difference between RPM group and control group(P 0.05).There was no difference of BDNF mRNA in hippocampus(P0.05) and in brain(P0.05) between RPM group and model group,but those of model group were lower than control group in hippocampus(P 0.05) and in brain(P 0.05).In the case of pro-BDNF,there was no difference between RPM group and model group in hippocampus(P0.05)and brain(P0.05),but those of model group were lower than those of control group in hippocampus(P 0.05) and in brain(P 0.05).Conclusions D-gal could induce the defect of learning and memory in rats,being related to the decrease of pro-BDNF in hippocampus and brain.RPM could delay the deterioration of learning and memory induced by D-gal,however,it could not change the expression of BDNF mRNA and the level of proBDNF.
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Objective To explore the influence of Radix Polygoni Multiflori(RPM) on brain-derived neurotrophic factor(BDNF) expression of hippocampus and brain in the senile rat induced by D-galactose(D-gal).Methods 36 rats were randomly divided into control,senile model and RPM groups.The model and RPM group were injected with D-gal 0.125 g·kg-1·d-1 by subcutaneous injection continuously for 60 days,while control group were administered with the same dose of normal saline per day.The ability of learning and memory of rats were measured in Morris water maze,the amount of mRNA of BDNF was measured by RT-PCR and the amount of protein of BDNF was measured by Western blot.Results The escape latency of model group was longer than that of control group(P 0.05),and there was no difference between RPM group and control group(P 0.05).There was no difference of BDNF mRNA in hippocampus(P0.05) and in brain(P0.05) between RPM group and model group,but those of model group were lower than control group in hippocampus(P 0.05) and in brain(P 0.05).In the case of pro-BDNF,there was no difference between RPM group and model group in hippocampus(P0.05)and brain(P0.05),but those of model group were lower than those of control group in hippocampus(P 0.05) and in brain(P 0.05).Conclusions D-gal could induce the defect of learning and memory in rats,being related to the decrease of pro-BDNF in hippocampus and brain.RPM could delay the deterioration of learning and memory induced by D-gal,however,it could not change the expression of BDNF mRNA and the level of proBDNF.
Key concepts: Hippocampus, Internal medicine, Endocrinology, Brain-derived neurotrophic factor, Saline, Morris water navigation task, Hippocampal formation, Cerebrum