ObjectiveTo investigate the effects of Qizhujianwei granules （QZJW） on abnormal proliferation and malignant transformation of gastric mucosal cells in rats with gastric intraepithelial neoplasia （GIN） and to explore the related mechanisms. MethodsA total of 80 SPF male Wistar rats were used. A GIN rat model was established using a four-factor comprehensive method consisting of methylnitronitrosoguanidine （MNNG）， ranitidine， irregular feeding patterns， and sodium salicylate. Except for the normal group， after successful modeling， the rats were randomly divided according to body weight into a model group， a Moluodan group （0.55 g·kg^-1）， and a QZJW group （7.34 g·kg^-1）， with 12 rats in each group. All groups were treated for 8 weeks. The general characteristics of the rats and morphological changes of the gastric mucosa were observed. Histopathological changes of the gastric mucosa were examined by hematoxylin-eosin （HE） staining. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of pepsinogenⅠ （PGⅠ）， pepsinogenⅡ （PGⅡ）， and gastrin （G-17）， as well as the expression level of transforming growth factor-β₁ （TGF-β₁） in gastric mucosal tissue， and the PGⅠ/PGⅡ ratio was calculated. Immunohistochemistry （IHC） was used to detect the localization and expression levels of proliferating cell nuclear antigen （Ki-67） and Vimentin in gastric mucosal tissue. Western blot analysis was used to determine the protein expression levels of Wnt family member 3A （Wnt3a）， β-catenin， CyclinD₁， proto-oncogene Cmyc， transforming growth factor-β receptor Ⅰ （TGFβRⅠ）， intracellular signaling transducers Smad2/3， phosphorylated （p）-Smad2/3， twist family transcription factor （Twist1）， and Vimentin in gastric mucosal tissue. ResultsCompared with the normal group， the model group showed characteristic changes including dim eyes， pale ears and claws， dark-red tongue， and reduced luster of the tail. The gastric mucosa appeared pale， with surface congestion and erosion. The gastric mucosal glands were disordered， the nuclear-to-cytoplasmic ratio increased， and local tumor cells were observed. Serum PGⅠ and PGⅡ levels and the PGⅠ/PGⅡ ratio were significantly decreased （P<0.01）， while the level of G-17 was significantly increased （P<0.01）. The protein expression levels of Ki-67， Wnt3a， β-catenin， CyclinD₁， Cmyc， TGF-β₁， TGFβRⅠ， Smad2/3， Twist1， and Vimentin in gastric mucosal tissue were significantly increased （P<0.05， P<0.01）， whereas the ratio of p-Smad2/3 to Smad2/3 was significantly decreased （P<0.05）. Compared with the model group， the general characteristics and gastric mucosal conditions of rats in the Moluodan group and the QZJW group were improved. HE staining showed that QZJW could effectively block the malignant progression of GIN. Serum PGⅠ and PGⅡ levels and the PGⅠ/PGⅡ ratio were significantly increased （P<0.05， P<0.01）， while the level of G-17 was significantly decreased （P<0.01）. The protein expression levels of Ki-67， Wnt3a， β-catenin， CyclinD₁， Cmyc， TGF-β₁， TGFβRⅠ， Smad2/3， Twist1， and Vimentin in gastric mucosal tissue were significantly decreased （P<0.05， P<0.01）. ConclusionQZJW have a therapeutic effect on rats with GIN. The mechanism may involve inhibition of the Wnt/β-catenin signaling pathway to regulate the cell cycle and suppress abnormal cell proliferation. Meanwhile， it may inhibit epithelial-mesenchymal transition by suppressing the TGF-β₁/Smad/Twist1 signaling pathway， thereby blocking the malignant progression of GIN.

ObjectiveTo investigate the effects of Qizhujianwei granules （QZJW） on abnormal proliferation and malignant transformation of gastric mucosal cells in rats with gastric intraepithelial neoplasia （GIN） and to explore the related mechanisms. MethodsA total of 80 SPF male Wistar rats were used. A GIN rat model was established using a four-factor comprehensive method consisting of methylnitronitrosoguanidine （MNNG）， ranitidine， irregular feeding patterns， and sodium salicylate. Except for the normal group， after successful modeling， the rats were randomly divided according to body weight into a model group， a Moluodan group （0.55 g·kg^-1）， and a QZJW group （7.34 g·kg^-1）， with 12 rats in each group. All groups were treated for 8 weeks. The general characteristics of the rats and morphological changes of the gastric mucosa were observed. Histopathological changes of the gastric mucosa were examined by hematoxylin-eosin （HE） staining. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of pepsinogenⅠ （PGⅠ）， pepsinogenⅡ （PGⅡ）， and gastrin （G-17）， as well as the expression level of transforming growth factor-β₁ （TGF-β₁） in gastric mucosal tissue， and the PGⅠ/PGⅡ ratio was calculated. Immunohistochemistry （IHC） was used to detect the localization and expression levels of proliferating cell nuclear antigen （Ki-67） and Vimentin in gastric mucosal tissue. Western blot analysis was used to determine the protein expression levels of Wnt family member 3A （Wnt3a）， β-catenin， CyclinD₁， proto-oncogene Cmyc， transforming growth factor-β receptor Ⅰ （TGFβRⅠ）， intracellular signaling transducers Smad2/3， phosphorylated （p）-Smad2/3， twist family transcription factor （Twist1）， and Vimentin in gastric mucosal tissue. ResultsCompared with the normal group， the model group showed characteristic changes including dim eyes， pale ears and claws， dark-red tongue， and reduced luster of the tail. The gastric mucosa appeared pale， with surface congestion and erosion. The gastric mucosal glands were disordered， the nuclear-to-cytoplasmic ratio increased， and local tumor cells were observed. Serum PGⅠ and PGⅡ levels and the PGⅠ/PGⅡ ratio were significantly decreased （P<0.01）， while the level of G-17 was significantly increased （P<0.01）. The protein expression levels of Ki-67， Wnt3a， β-catenin， CyclinD₁， Cmyc， TGF-β₁， TGFβRⅠ， Smad2/3， Twist1， and Vimentin in gastric mucosal tissue were significantly increased （P<0.05， P<0.01）， whereas the ratio of p-Smad2/3 to Smad2/3 was significantly decreased （P<0.05）. Compared with the model group， the general characteristics and gastric mucosal conditions of rats in the Moluodan group and the QZJW group were improved. HE staining showed that QZJW could effectively block the malignant progression of GIN. Serum PGⅠ and PGⅡ levels and the PGⅠ/PGⅡ ratio were significantly increased （P<0.05， P<0.01）， while the level of G-17 was significantly decreased （P<0.01）. The protein expression levels of Ki-67， Wnt3a， β-catenin， CyclinD₁， Cmyc， TGF-β₁， TGFβRⅠ， Smad2/3， Twist1， and Vimentin in gastric mucosal tissue were significantly decreased （P<0.05， P<0.01）. ConclusionQZJW have a therapeutic effect on rats with GIN. The mechanism may involve inhibition of the Wnt/β-catenin signaling pathway to regulate the cell cycle and suppress abnormal cell proliferation. Meanwhile， it may inhibit epithelial-mesenchymal transition by suppressing the TGF-β₁/Smad/Twist1 signaling pathway， thereby blocking the malignant progression of GIN.

Medical parasitology, as a course bridging basic medical sciences and clinical medicine, has an important disciplinary value in the medical education system. This study investigated the composition of parasitology teachers from multiple medical colleges and universities across China. The results showed that there was a significant difference in the proportion of teachers with clinical medicine background knowledge, and there was common dilemma that there were insufficient clinical medicine knowledge reserves among teachers in some medical colleges and universities, who encountered severe teaching challenges. Based on this issue, this study constructed a basic-clinical medicine collaborative problem-based learning (PBL) teaching model. This model integrated theoretical teaching, case analyses, and experimental operations, and combined transdisciplinary team building and multidimensional teacher training, which significantly improved the clinical teaching capability among parasitology teachers, and effectively compensated the impact of insufficient clinical medicine knowledge reserves on teaching. Following teaching reform, students' scores significantly improved, and their case analysis capability enhanced. This study provides a practical path to address the shortage of clinical medicine background knowledge among parasitology teachers, which facilitates the progress of educational reform of medical parasitology and improvement of teaching quality.

ObjectiveTo explore the effect of the medical-community linkage model on activities of daily living, psychological status and motor function of stroke patients in the community. MethodsA total of 60 stroke patients admitted to two community health service centers and their affiliated stations in Fengtai District, Beijing, from January, 2024 to August, 2025 were enrolled and randomly divided into control group (n = 30) and intervention group (n = 30). The control group received routine medicine, dietary care and rehabilitation management, while the intervention group underwent rehabilitation with the medical-community linkage model, for twelve weeks. They were assessed with modified Barthel Index (MBI), Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD) and Fugl-Meyer Assessment (FMA) before and after intervention. ResultsAfter intervention, the MBI, HAMA, HAMD and FMA scores of patients improved in both groups (|t| > 5.599, P < 0.001), and improved more in the intervention group than in the control group (P < 0.05), except MBI. The HAMA and HAMD scores of family members decreased in both groups (|t| > 10.333, P < 0.001), and decreased more in the intervention group than in the control group (t > 5.681, P < 0.001). ConclusionThe medical-community linkage model can further improve the motor function of stroke patients in community, as well as the psychological status of both patients and their family members.

AIM:To investigate the effects of Xiaoyao-Kang'ai-Jieyu formula(XYKAJY)-containing serum on the co-culture of BV2 and HT22 cells from mice with breast cancer-related depression(BCRD).METHODS:The op-timal concentration of XYKAJY-containing serum was determined using mouse HT22 cells.In vitro co-culture model of mouse HT22 and BV2 cells was established through incubation with 4T1 cell supernatant and 200 μmol/L corticosterone.The cells were then divided into control group,model group,blank serum group,positive drug serum group,5%XY-KAJY-containing serum group,10%XYKAJY-containing serum group,15%XYKAJY-containing serum group and 20%XYKAJY-containing serum group.Alterations in HT22 cell viability was detected by CCK8 assay.The concentration level of interleukin-1β(IL-1β),IL-6 and IL-18 in the cell supernatant was quantified using enzyme-linked immunosorbent as-say(ELISA).Flow cytometry was conducted to assess the apoptosis rate of HT22 cells and quantify the expression levels of adhesion molecule CD11b on the surface of BV2 cells.Immunofluorescence was performed to determine the expression of neuron-specific enolase(NSE),synapsin 1(Syn1)and postsynaptic density protein 95(PSD95)in HT22 cells,and that of inducible nitric oxide synthase(iNOS)in BV2 cells.RESULTS:Treatment with XYKAJY-containing serum down-regulated CD11b expression level in BV2 cells(P<0.01),and reduced the release of IL-1β,IL-6 and IL-18(P<0.01).Moreover,it significantly improved the viability of HT22 cells(P<0.01),enhanced cell morphology integrity,and reduced the apoptosis rate(P<0.01).CONCLUSION:These findings indicated that XYKAJY-containing serum im-proved the function of mouse HT22 neurons by regulating the polarization phenotype of mouse BV2 cells and alleviating neuroinflammatory-induced toxicity.

Objective:This study aimed to evaluate the feasibility and safety of surgical intervention for patients with stage Ⅳ esophageal cancer who demonstrated tumor regression following first-line treatment.Methods:This was a descriptive case series. The inclusion criteria for surgery were as follows: (1) an initial diagnosis of stage Ⅳ esophageal cancer, i.e. cT4b or cM1; (2) the presence of residual tumor following first-line therapy deemed potentially resectable upon reassessment; and (3) sufficient organ function to tolerate surgical procedures. Clinical data were retrospectively collected for 63 patients with stage Ⅳ esophageal cancer who underwent surgery following first-line therapy at Sun Yat-sen University Cancer Center between January 2014 and December 2023. Of these patients, 12 were initially staged as IVA, and 51 as IVB. Post-treatment restaging revealed that 9 patients achieved a clinical complete response, while 3 were downstaged to stage Ⅰ, 14 to stage Ⅱ, 24 to stage Ⅲ, and 13 to stage ⅣB (with regression of distant metastatic lesions enabling curative resection). Surgical approaches included right thoracic esophagectomy ( n=55), left thoracic esophagectomy ( n=4), and transmediastinal esophagectomy ( n=4). Additionally, 7 patients required extended organ resection. Two-field lymph node dissection was performed in 49 patients, while 14 underwent three-field lymph node dissection. Postoperative management varied: 31 patients received no adjuvant therapy, 11 underwent immunochemotherapy, 8 received immunotherapy alone, 8 underwent chemotherapy, 4 received chemoradiotherapy, and 1 received combined radiotherapy and immunotherapy. The primary endpoints were overall survival (OS) and progression-free survival (PFS), with secondary endpoints including surgical outcomes and postoperative complications. Results:All 63 patients successfully underwent surgery without intraoperative mortality. R0 resection was achieved in 58 cases (92.1%), while R1 and R2 resections were performed in 1 case (1.6%) and 4 cases (6.3%), respectively. The mean operative time was 357±135 minutes. Postoperative complications were observed in 27 cases (42.9%), with 9 cases (14.3%) classified as Clavien-Dindo grade Ⅲ or Ⅴ. One patient (1.6%) died perioperatively. The median follow-up duration was 21 months (range: 4–107 months). The median OS was 64.8 months (95% CI: 50.9–78.6 months), and the median PFS was 68.0 months (95% CI: 53.9–82.3 months). Among 24 patients with supraclavicular lymph node metastases, 6 experienced recurrence and 8 died. Of 25 patients with abdominal metastases, 3 had recurrence and subsequently died. All 4 patients with lung metastases and both patients with bone metastases experienced recurrence and death.Conclusions:Surgical intervention is a feasible and safe treatment option for selected patients with stage Ⅳ esophageal cancer who demonstrate the potential for curative resection following first-line therapy.

Objective To explore the effect and mechanism of Zuogui Jiangtang Jieyu Formula(ZGJTJYF)in treating diabetes-related depression by regulating glutamate receptor 2(GluR2).Methods The primary isolated and cultured hippocampal neurons of SD rats were used.The experiment consisted of normal,model,blank serum(10％blank serum),positive drug(10％[metformin+fluoxetine]drug-containing serum),20％ZGJTJYF group,10％ZGJTJYF group,10％ZGJTJYF+GluR2 knockdown group,and 10％ZGJTJYF+GluR2 overexpression group(with corresponding volume fractions of ZGJTJYF drug-containing serum added).The ZGJTJYF+GluR2 knockdown and overexpression groups,were transfected with lentivirus to obtain hippocampal neurons with either GluR2 overexpression or knockdown.The glucose(150 mmol/L)and corticosterone(200 μmol/L)were used for 18 h to establish an in vitro cell model of hippocampal neurons in diabetes-related depression.After 24 h of successful modeling,the corresponding serum was added to each group for intervention.After 24 h of intervention,the morphological structure of hippocampal neurons was observed using an optical microscope.Biochemical methods were used to determine the glucose and insulin content in cell supernatant.An enzyme-linked immunosorbent assay was used to detect 5-hydroxytryptamine(5-HT)and dopamine(DA)levels in the cell supernatant,and the microtubule-associated protein 1A/1B light chain 3 autophagy double-labeled adenovirus(mRFP-GFP-LC3)autophagy fluorescence double labeling method was used to detect the average fluorescence intensity of LC3 protein in hippocampal neurons.Nissl staining was used to observe synaptic damage in hippocampal neurons,and an immunofluorescence method was used to detect the protein expression of Parkin,phosphatase and tensin homolog-induced putative kinase 1(PINK1),regulating synaptic membrane exocytosis 3(RIMS3),synapsin 1(SYN1),postsynaptic density-95(PSD-95),synapse-associated protein 102(SAP 102),and GluR2 in hippocampal neurons.Realtime fluorescence PCR was used to detect GluR2 mRNA expression in hippocampal neurons,while Western blotting was employed to assess the expression of mitophagy proteins Parkin and PINK1 in these neurons.Results Compared to the normal group,the model group and blank serum group showed structural damage to hippocampal neurons,increased glucose content in cell supernatant,decreased insulin,5-HT,and DA content,increased average fluorescence intensity of LC3,Parkin,and PINK1,decreased average fluorescence intensity of RIMS3,SYN1,PSD-95,SAP 102,and GluR2,decreased GluR2 mRNA expression,increased protein expression of Parkin and PINK1(P＜0.05),and decreased Nissl bodies.Compared to the model group and blank serum group,the above indicators in each administration group were improved to varying degrees(P＜0.05).Compared to the positive drug group,the average fluorescence intensity of LC3,Parkin,and PINK1 decreased,Parkin and PINK1 protein expression decreased,and the average fluorescence intensity of GluR2,SYN1,and PSD-95 increased in 10％ZGJTJYF,20％ZGJTJYF group,and 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％and 20％ZGJTJYF groups,10％ZGJTJYF+GluR2 knockdown group showed a decrease in 5-HT content,an increase in average fluorescence intensity of LC3 and Parkin,a decrease in average fluorescence intensity of SYN1,PSD-95,and GluR2,a decreased in GluR2 mRNA expression,and an increase of Parkin and PINK1 protein expression(P＜0.05).In contrast,the above indicators were improved to varying degrees in 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％ZGJTJYF+GluR2 knockdown group,the above abnormal indicators in 10％ZGJTJYF+GluR2 overexpression group were reversed to varying degrees(P＜0.05).Conclusion ZGJTJYF has a protective effect on synaptic damage of hippocampal neurons in diabetes-related depression,and its mechanism may be related to the upregulation of GluR2 and the inhibition of mitophagy over activation.

Objective:To explore the current status and trends in emergency nursing teaching methods based on CiteSpace software in China from 2012 to 2023, and to provide reference for subsequent research.Methods:Literature on teaching methods in emergency nursing was electronically searched in the China National Knowledge Infrastructure, WanFang Data, and VIP from January 2012 to December 2023. CiteSpace and Excel software were used to perform bibliometric analysis on the publication year, journal source, first author affiliation, keywords and clustering content.Results:An initial search yielded 1 550 articles and 936 relevant articles were screened and published in 194 journals. From 2012 to 2023, the number of publications on teaching methods in emergency nursing in China was relatively flat, the first author affiliations were mainly general hospitals, and the research methods were mainly quantitative. Keyword clustering showed that six themes were extracted, including exploration of professional skills, reform and application of teaching methods, nursing teaching and evaluation, teaching modes, teaching tools, and training modes.Conclusions:The trend of publications in emergency nursing teaching methods in China in the past 10 years has been relatively flat, and the quality of the literature needs to be improved. Emergency nursing teaching needs to focus on reforming teaching modes and methods, and further exploring the use of tools such as mind maps and teaching manuals to improve the quality of teaching.

Objective To explore the effect and mechanism of Zuogui Jiangtang Jieyu Formula(ZGJTJYF)in treating diabetes-related depression by regulating glutamate receptor 2(GluR2).Methods The primary isolated and cultured hippocampal neurons of SD rats were used.The experiment consisted of normal,model,blank serum(10％blank serum),positive drug(10％[metformin+fluoxetine]drug-containing serum),20％ZGJTJYF group,10％ZGJTJYF group,10％ZGJTJYF+GluR2 knockdown group,and 10％ZGJTJYF+GluR2 overexpression group(with corresponding volume fractions of ZGJTJYF drug-containing serum added).The ZGJTJYF+GluR2 knockdown and overexpression groups,were transfected with lentivirus to obtain hippocampal neurons with either GluR2 overexpression or knockdown.The glucose(150 mmol/L)and corticosterone(200 μmol/L)were used for 18 h to establish an in vitro cell model of hippocampal neurons in diabetes-related depression.After 24 h of successful modeling,the corresponding serum was added to each group for intervention.After 24 h of intervention,the morphological structure of hippocampal neurons was observed using an optical microscope.Biochemical methods were used to determine the glucose and insulin content in cell supernatant.An enzyme-linked immunosorbent assay was used to detect 5-hydroxytryptamine(5-HT)and dopamine(DA)levels in the cell supernatant,and the microtubule-associated protein 1A/1B light chain 3 autophagy double-labeled adenovirus(mRFP-GFP-LC3)autophagy fluorescence double labeling method was used to detect the average fluorescence intensity of LC3 protein in hippocampal neurons.Nissl staining was used to observe synaptic damage in hippocampal neurons,and an immunofluorescence method was used to detect the protein expression of Parkin,phosphatase and tensin homolog-induced putative kinase 1(PINK1),regulating synaptic membrane exocytosis 3(RIMS3),synapsin 1(SYN1),postsynaptic density-95(PSD-95),synapse-associated protein 102(SAP 102),and GluR2 in hippocampal neurons.Realtime fluorescence PCR was used to detect GluR2 mRNA expression in hippocampal neurons,while Western blotting was employed to assess the expression of mitophagy proteins Parkin and PINK1 in these neurons.Results Compared to the normal group,the model group and blank serum group showed structural damage to hippocampal neurons,increased glucose content in cell supernatant,decreased insulin,5-HT,and DA content,increased average fluorescence intensity of LC3,Parkin,and PINK1,decreased average fluorescence intensity of RIMS3,SYN1,PSD-95,SAP 102,and GluR2,decreased GluR2 mRNA expression,increased protein expression of Parkin and PINK1(P＜0.05),and decreased Nissl bodies.Compared to the model group and blank serum group,the above indicators in each administration group were improved to varying degrees(P＜0.05).Compared to the positive drug group,the average fluorescence intensity of LC3,Parkin,and PINK1 decreased,Parkin and PINK1 protein expression decreased,and the average fluorescence intensity of GluR2,SYN1,and PSD-95 increased in 10％ZGJTJYF,20％ZGJTJYF group,and 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％and 20％ZGJTJYF groups,10％ZGJTJYF+GluR2 knockdown group showed a decrease in 5-HT content,an increase in average fluorescence intensity of LC3 and Parkin,a decrease in average fluorescence intensity of SYN1,PSD-95,and GluR2,a decreased in GluR2 mRNA expression,and an increase of Parkin and PINK1 protein expression(P＜0.05).In contrast,the above indicators were improved to varying degrees in 10％ZGJTJYF+GluR2 overexpression group(P＜0.05).Compared to 10％ZGJTJYF+GluR2 knockdown group,the above abnormal indicators in 10％ZGJTJYF+GluR2 overexpression group were reversed to varying degrees(P＜0.05).Conclusion ZGJTJYF has a protective effect on synaptic damage of hippocampal neurons in diabetes-related depression,and its mechanism may be related to the upregulation of GluR2 and the inhibition of mitophagy over activation.

ObjectiveTo reveal the mechanism of Zuogui Jiangtang Jieyu prescription against damage to hippocampal synaptic microenvironment via suppressing glutamate receptor 2 （GluR2）/Parkin signal-mediated mitophagy in rats with diabetes-related depression （DD）. MethodsEighty male SD rats underwent adaptive feeding for 5 days before the study. Ten rats were randomly assigned to the normal group. The model of DD rats was established with the rest by 2-week high-fat diet + streptozotocin （STZ） tail intravenous injection + 28 days of chronic unpredictable mild stress （CUMS） combined with isolation. The rats were randomly divided into a normal group， a model group， a GluR2 blocker group （5 μg·kg^-1）， a GluR2 agonist group （10 μg·kg^-1）， a metformin + fluoxetine group （0.18 g·kg^-1 metformin + 1.8 mg·kg^-1 fluoxetine）， and high- and low-dose Zuogui Jiangtang Jieyu prescription groups （20.52 and 10.26 g·kg^-1， respectively）. The rats in the GluR2 blocker group and the GluR2 agonist group were continuously injected with CNQX and Cl-HIBO in the dentate gyrus of the hippocampus once a week starting from stress modeling， respectively， while the metformin + fluoxetine group and the high- and low-dose Zuogui Jiangtang Jieyu prescription groups were continuously given intragastric administration for 28 d at the same time of stress modeling. Depression-like behavior was evaluated by open field and forced swimming experiments. The levels of serum insulin and adenosine triphosphate （ATP） in hippocampus were detected by biochemical analysis. The levels of 5-hydroxytryptamine （5-HT） and dopamine （DA） in hippocampus were detected by enzyme-linked immunosorbent assay （ELISA）. The autophagosomes of hippocampal neurons were observed by transmission electron microscopy. The morphology and structure of dendrites and spines of hippocampal neurons were evaluated by Golgi staining. Western blot detected the expression levels of GluR2 and Parkin proteins in hippocampus. The expression levels of GluR2， Parkin， regulating synaptic membrane exocytosis protein 3 （RIMS3）， and postsynaptic density protein 95 （PSD95） in the dentate gyrus of the hippocampus were detected by immunofluorescence. ResultsCompared with the normal group， the model group exhibited reduced total activity distance in the open field and increased immobility time in forced swimming （P<0.01）， lowered levels of serum insulin and ATP， 5-HT， and DA in hippocampus （P<0.01）， increased autophagosomes of hippocampal neurons， significantly damaged morphology and structure of dendrites and spines of hippocampal neurons， decreased expression levels of GluR2， RIMS3， and PSD95 in hippocampus， and an increased Parkin expression level （P<0.05， P<0.01）. Compared with the model group， the GluR2 blocker group and the GluR2 agonist group showed aggravation and alleviation of the above abnormal changes， respectively （P<0.05， P<0.01）. The above depression-like behavior was significantly improved in the high- and low-dose Zuogui Jiangtang Jieyu prescription groups to different degrees. Specifically， the two groups saw elevated levels of serum insulin and ATP， 5-HT， and DA in hippocampus （P<0.05， P<0.01）， restrained increase in autophagosomes and damage to morphology and structure of dendrites and spines of hippocampal neurons， up-regulated protein expression levels of GluR2， RIMS3， and PSD95， and down-regulated Parkin expression level （P<0.05， P<0.01）. ConclusionZuogui Jiangtong Jieyu prescription can ameliorate the mitophagy-mediated damage to hippocampal synaptic microenvironment in DD rats， the mechanism of which might be related to the regulation of GluR2/Parkin signaling pathway.