Amygdalin ameliorates post-stroke depression by inhibiting JNK signal pathway
Objective To study the ameliorative effect of amygdalin on post-stroke depression by inhibiting JNK signal pathway.Methods A total of 30 healthy SD rats were randomly divided into sham operation group(n=8),model group 1(n=8)and model group 2(n=40).Stroke models were made in group 1,and post-stroke depression models were made in group 2.After successful modeling,the post-stroke depression model rats were randomly divided into stroke+depression group,stroke+depression+amygdalin low dose group(40 mg·kg-1),stroke+depression+amygdalin medium dose group(80 mg·kg-1),stroke+depression+amygdalin high dose group(120 mg·kg-1),and stroke+depression+fluoxetine group(1.8 mg·kg-1).Then the drug was given according to the corresponding dose for 30 days.The Zea Longa score and sucrose water consumption were observed;the pathological changes of hippocampal tissue were observed by H&E staining;the neuronal apoptosis was observed by TUNEL staining;the ultrastructural changes of hippocampal tissue were observed by transmission electron microscope,and Western blot was used to detect the expression of PSD95,SYN,BDNF and JNK,p-JNK,c-Jun,p-c-Jun,cleaved-caspase 3 and Bcl-2 protein in hippocampal tissue.Results Compared with the sham operation group,the Zea Longa neurobehavioral score,the percentage of apoptosis and the expression of p-JNK,c-Jun and p-c-Jun protein in hippocampus were significantly increased,while the sucrose water consumption,PSD95,SYN,BDNF and Bcl-2 protein expressions in hippocampus were significantly decreased in stroke group and stroke+depression group(P<0.05).Compared with the stroke+depression group,Zea Longa neurobehavioral scores,apoptosis percentage and hippocampal tissue p-JNK,c-Jun,p-c-Jun,cleaved-caspase 3 protein expression was significantly decreased(P<0.05),and sucrose water consumption,hippocampal tissue PSD95,SYN,BDNF,and Bcl-2 protein expression were significantly increased in stroke+depression+amygdalin low dose group,stroke+depression+amygdalin medium dose group,stroke+depression+amygdalin high dose group,and stroke+depression+fluoxetine group(P<0.05).Compared with the stroke+depression+fluoxetine group,Zea Longa neurobehavioral score,apoptosis percentage and hippocampal tissue p-JNK,c-Jun,p-c-Jun,cleaved-caspase 3 protein expression were significantly decreased(P<0.05),and hippocampal tissue PSD95,SYN,BDNF,and Bcl-2 protein expressions were significantly increased in the stroke+depression+amygdalin high-dose group(P<0.05).Conclusion Amygdalin improves depression-like behavior after stroke,which may be related to the inhibition of hippocampal JNK signal pathway.