Effect of gastrodin on cognition and hippocampal tissue damage in rats with schizophrenia by regulating the CREB/BDNF signaling pathway
Objective To explore the repair ability of gastrodin(GAS)on neuronal damage in rats with schizophrenia(SCH)and its impact on cAMP-response element binding protein/brain-derived neurotrophic factor(CREB/BDNF)signaling pathway.Methods A SCH rat model was constructed using MK-801 and randomly divided into model group,low-dose GAS gourp(GAS-L group),high-dose GAS group(GAS-H group),and a high-dose GAS+pathway inhibitor group(GAS-H+H89 group),with 10 rats in each group.Additional 10 healthy rats were selected as control group.All rats were rated for stereotypical behavior and Morris water maze scores.HE staining was applied to observe the morphology of hippocampal tissue.TUNEL staining was applied to observe the apoptosis of hippocampal neurons.ELISA was applied to detect levels of serum oxidative stress factors.Western blot was applied to detect the expression of proteins related to the CREB/BDNF signaling pathway.Results Compared with control group,the hippocampal tissue cells of rats in model group showed disordered arrangement,extensive loss of neurons,overall structural damage,the increased behavioral score and cell apoptosis rate,the extended escape latency,the shortened platform stay time,and the decreased levels of oxidative stress factors(CAT,SOD,GSH-Px)and p-CREB,CREB,and BDNF proteins(P＜0.05).Compared with model group,with the increase of GAS dose,the pathological damages of hippocampal tissue of rats in GAS-L and GAS-H groups were reduced,the behavioral scores and cell apoptosis rates decreased,the escape latencys shortened,the platform stay time prolonged,and the levels of oxidative stress factors(CAT,SOD,GSH-Px)and p-CREB,CREB,and BDNF proteins increased(P＜0.05).Compared with GAS-H group,the pathological damage to the hippocampal tissue of rats in GAS-H+H89 group worsened,the behavioral score and cell apoptosis rate increased,the escape latency extended,the platform stay time shortened,and the levels of oxidative stress factors(CAT,SOD,GSH-Px)and p-CREB,CREB,and BDNF proteins decreased(P＜0.05).Conclusion GAS can improve neuronal damage in SCH rats,which may be related to the regulation of the CREB/BDNF signaling pathway.
GastrodinSchizophreniaNeurological damagecAMP-response element binding protein/brain-derived neurotrophic factor signaling pathway
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