Study On Mechanism Of CGJY In The Intervention Of Post-stroke Depression

Objective: The mechanism of action of CGJY in post-stroke depression model rats was scientifically evaluated by examining the behavior of rats,detecting serum inflammatory factors,observing cell morphology in hippocampal region,and detecting proteins related to autophagy signaling pathway and BDNF/ERK/CREB signaling pathway in hippocampal region.Methods: SPF-grade SD rats were divided into 5 groups(Normal、PSD、CGJYL、CGJYH、Fluoxetine),and the PSD model was prepared by MCAO combined with chronic unpredictable mild stimulation + single cage solitary feeding method.The normal and PSD model groups were given saline gavage,the herbal treatment group was given CGJY aqueous decoction by gavage,and the fluoxetine group was given fluoxetine suspension by gavage for 21 d.The general status of rats such as hemiparesis was observed;the changes in body weight of rats were measured;the behavioral changes of rats were detected by open box test and neurological deficit score;the serum inflammatory factors IL-1β,IL-6 and TNF-α were detected by ELISA.The cell morphology of rat hippocampus was observed by HE staining;the expression of autophagy signaling pathway proteins Beclin 1,LC3 and BDNF/ERK/CREB signaling pathway related proteins in rat hippocampus was detected by Western blotting.Results:1.General status,body weight and behavioral results: compared with the normal group,rats in the PSD model group showed depressed mental status,hemiparesis,decreased body weight(p<0.01),decreased open box test score(p<0.01)and increased neurological deficit score(p<0.01).Compared with the PSD model group,the rats in the herbal treatment group showed improved mental status,reduced hemiparesis,increased body weight(p<0.05),increased open box test score(p<0.05),and decreased neurological deficit score(p<0.01).2.The results of serum inflammatory factor determination: compared with the normal group,the serum IL-1β,IL-6 and TNF-α levels of rats in the PSD model group were significantly higher(p<0.01);compared with the PSD model group,the serum IL-1β,IL-6and TNF-α levels of rats in the herbal treatment group were significantly lower(p<0.05).3.The results of HE staining and expression of autophagy signaling pathway-related proteins in the rat hippocampus: compared with the normal group,the hippocampal neurons in the PSD model group were significantly reduced in number,unevenly arranged,with more necrotic cells and partially atrophied and deformed;the expression of Beclin 1 and LC3-II/LC3-I in hippocampal tissue was increased(p<0.01).Compared with the PSD model group,the number of hippocampal neurons increased,the arrangement tended to be uniform,the number of necrotic cells was less,and the morphological structure was normal;the expression of Beclin 1 and LC3-II/LC3-I in hippocampal tissues were significantly reduced(p<0.01).4.The results of BDNF/ERK/CREB signaling pathway-related protein expression in rat hippocampus: compared with the normal group,the expression of BDNF,p-ERK/ERK and CREB in hippocampal tissue of rats in the PSD model group was decreased(p<0.01).Compared with the PSD model group,the expression of BDNF,p-ERK/ERK and CREB in hippocampal tissue of rats in the herbal treatment group were significantly increased(p<0.01).Conclusion:1.CGJY can improve the general status of PSD rats,including hemiplegia and depression,increase body weight and improve behavioral changes,thus enhancing their mobility and interest in activities.2.CGJY can inhibit the excessive inflammatory response of PSD by reducing the serum inflammation index in PSD rats.3.CGJY can promote neurological recovery,reduce the expression level of autophagic signaling pathway-related proteins in the hippocampal region of PSD rats,and prevent excessive autophagy of hippocampal neurons to protect the nervous system and reduce the degree of injury.4.CGJY can inhibit post-ischemic neurological injury in PSD rats by up-regulating the expression of proteins related to BDNF/ERK/CREB signaling pathway in the hippocampus.