Objective:To analyze the external quality control assessment results of fluoride testing laboratories in endemic disease prevention and control institutions nationwide from 2006 to 2023, investigate the quality control capabilities of these laboratories in various provinces, prefectures, cities, and counties nationwide, and ensure the accuracy and reliability of surveillance data on endemic fluorosis nationwide.Methods:Using retrospective analysis, the external quality control assessment results of all participating fluoride testing laboratories of national endemic disease prevention and control institutions from 2006 to 2023 were summarized and analyzed. The assessment results from 2006 to 2008 were tested for outliers using Grubbs method, homogeneity of variance using Cochran method, excluding the assessment data of unqualified laboratories, calculating the total mean and total standard deviation, Z-score method was used to test the assessment of laboratories, and statistical analysis and judgment were done when the result of │Z│ < 3. The assessment results from 2009 - 2023 were obtained from all laboratories. In 2010, two tests were conducted in the first and second half of the year, and the Z-ratio scores of each laboratory were calculated using robust statistics. When │Z│≤2, the assessment was qualified; when 2 < │Z│ < 3, the assessment was basically qualified; when│Z│≥3, the assessment was unqualified, and the consensus value came from all participating laboratories in the assessment.Results:From the beginning of quality control operation in 2006 to 2023, the number of laboratories participated in external quality control assessments had significantly increased. The number of laboratories participated in water fluoride assessment increased from 30 in 2006 to 1 277 in 2023, and the number of laboratories participated in urine fluoride assessment increased from 29 to 497. The number of laboratories participated in the brick tea fluorine assessment had increased from 43 in 2014 to 193 in 2023. The assessment results showed that when │Z│ < 3, the total qualified rate of fluoride external quality control in fluoride testing laboratories of national endemic disease control institutions was 95.2%, with the lowest being 87.1% (27/31) in 2008 and the highest being 100.0% (394/394) in 2014. When │Z│≤2, the total feedback pass rate was 88.4%, with the lowest being 79.3% (288/363) in the first half of 2010 and the highest being 99.5% (392/394) in 2014. The assessment results showed that when │Z│ < 3, the total pass rate of urine fluoride external quality control in fluoride testing laboratories of national endemic disease control institutions was 98.0%, with the lowest being 86.2% (25/29) in 2006 and 2007, respectively, and the highest being 100.0% (68/68) in 2014. When │Z│≤2, the total qualification rate was 93.7%, with the lowest being 86.5% (64/74) in the second half of 2010 and the highest being 100.0% (68/68) in 2014. The assessment results showed that when│Z│ < 3, the total pass rate of extra-fluoride quality control of brick tea in fluoride testing laboratories of national endemic disease control institutions was 95.4%, with the lowest being 85.0% (164/193) in 2023, and the highest being 100.0% (43/43, 51/51, 79/79) in 2014, 2015 and 2016, respectively. When │Z│≤2, the total pass rate was 89.2%, with the lowest being 72.7% (32/44) in 2017 and the highest being 100.0% (43/43) in 2014. From 2009 to 2023, there were a total of 21 provincial-level laboratories that passed the water fluoride detection assessment, including 3 provinces where all prefecture level and county-level laboratories were qualified. The assessment results of urinary fluorine showed that there were 11 qualified provincial-level laboratories and 1 prefecture-level laboratory. From 2014 to 2023, the assessment results of brick-tea fluorine showed that there were 5 provincial-level laboratories that passed the tea fluorine testing assessment and no prefecture-level laboratory.Conclusions:Conclusion: From 2006 to 2023, the number of fluoride testing laboratories participating in external quality control assessment has increased year by year, and most provincial, municipal and county-level laboratories have good fluoride testing capabilities, which can meet the testing needs of endemic disease prevention and monitoring. For some laboratories with problems, targeted rectification should be carried out to improve the quality of detection, in order to provide better technical support for the monitoring of endemic fluorosis areas.

Ankylosing spondylitis (AS) combined with lower cervical fracture is often categorized into unstable fracture, with a high incidence of neurological injury and a high rate of disability and morbidity. As factors such as shoulder occlusion may affect the accuracy of X-ray imaging diagnosis, it is often easily misdiagnosed at the primary diagnosis. Non-operative treatment has complications such as bone nonunion and the possibility of secondary neurological damage, while the timing, access and choice of surgical treatment are still controversial. Currently, there are no clinical practice guidelines for the treatment of AS combined with lower cervical fracture with or without dislocation. To this end, the Spinal Trauma Group of Orthopedics Branch of Chinese Medical Doctor Association organized experts to formulate Clinical guidelines for the treatment of ankylosing spondylitis combined with lower cervical fracture in adults ( version 2024) in accordance with the principles of evidence-based medicine, scientificity and practicality, in which 11 recommendations were put forward in terms of the diagnosis, imaging evaluation, typing and treatment, etc, to provide guidance for the diagnosis and treatment of AS combined with lower cervical fracture.

This article introduces an overview of management system for conflict of interest of the European Pharmacopoeia Commission (EPC) and the United States Pharmacopoeia Convention (USP). The EPC and USP have standardized the management system for conflict of interest in drug standard work in multiple management documents, such as the Guide for the Work, Code of Practice for the Work, Form for Declaration of Interests and Confidentiality Undertaking of the EPC, bylaws, Rules and Procedures of the Council of Experts, Code of Ethics, Standards of Conduct of the USP, in order to ensure the transparency and fairness of drug standard development, improve the credibility and rigor of drug standards. This article introduces the management system for conflict of interest of the EPC and USP, providing reference for the improvement of relevant management systems of the Chinese Pharmacopoeia Commission.

The study utilized spectral correlation analyses combined with bioactivity evaluation to examine the effective components of antidepressants in the Baihe Dihuang decoction. Firstly, the chemical fingerprints for different extraction parts in the Baihe Dihuang decoction were achieved using HPLC and UHPLC-MS technology. Then, in order to evaluate the antidepressant effect of Baihe Dihuang decoction, the animal experimental protocol has been reviewed and approved by Laboratory Animal Ethics Committee of Hunan University of Chinese Medicine (No. LLBH-202104270001), in compliance with the Institutional Animal Care Guidelines. We recorded the distance of autonomous movement of mice in open field experiment, the immobility time of tail suspension test, and the forced swimming. Additionally, we measured the content of neurotransmitters. Finally, Pearson analysis, grey correlation analysis, and orthogonal partial least squares regression analysis were utilized to establish the correlation between antidepressant efficacy indicators and fingerprinting. The spectrum-effect relationship results were confirmed through the in vitro activity verification. This study demonstrated that regaloside A, B, C, catalpol, and Isoacteoside might be the main antidepressant components in Baihe Dihuang decoction. Furthermore, it was found that using diverse mathematical models and bioactivity evaluation could enhance the accuracy of the spectral correlation analyses results.

Objective To explore the protective mechanism of Zuogui Jiangtang Jieyu Formula(ZGF)on synaptic damage of hippocampal neurons based on leukocyte mono-immunoglobulin-like receptor 3(CD300f)/glucose transporter 1(GLUT1)signal-mediated microglial glucose metabolism in rats with diabetes-related depression.Methods Eighty male SD rats were randomly selected using random number table method,with 10 rats serving as the normal group.The remaining 70 rats were fed a high-fat diet for 4 weeks and then injected once with 38 mg/kg of streptozotocin via the tail vein to replicate the diabetes rat model.Sixty rats were screened and successfully modeled,which were randomly divided into the model,CD300f blocker,CD300f agonist,metformin+fluoxetine(metformin 0.18 g/kg+fluoxetine 1.8 mg/kg),and ZGF high-and low-dose(20.52 and 10.26 g/kg,respectively)groups using random number table method.In addition to the normal group,the rats in the other groups underwent chronic unpredictable mild stress combined with isolation feeding for 28 days to replicate the diabetes-related depression rat model.The metformin+fluoxetine and ZGF high-and low-dose groups were subjected to continuous intragastrial administration for 14 days after the second week of modeling.The normal and model groups were administered an equal amount of distilled water by gavage.The CD300f blocker group and agonist group received microinjection into the hippocampus,with injection of myeloid cell trigger receptor inhibitory factor(CLM1,2 μg/kg)and immunoglobulin Fc surface protein(Fcγ,5 μg/kg)once a week,respectively.Depression-like behavior in rats was evaluated using open-field and forced swimming tests after the intervention.Biochemical analysis was used to detect the glucose,lactic acid,and adenosine diphosphate(ADP)/adenosine triphosphate(ATP)ratio contents.The insulin,5-hydroxytryptamine(5-HT),and dopamine(DA)levels in the hippocampus were detected using an enzyme-linked immunosorbent assay.Immunofluorescence was used to detect the average fluorescence intensity of CD300f,GLUT1,regulating synaptic membrane wxocytosis 3(RIMS3),and synapse-associated protein 102(SAP102)in hippocampal tissue.Western blotting was used to detect the CD300f,GLUT1,RIMS3,and SAP102 protein expression levels in the hippocampus.The synaptic damage of hippocampal neurons was observed using Nissl staining and transmission electron microscope.Results Compared with the normal group,the model group showed a decrease in the total active distance in the open-field test and an increase in forced swimming immobility time,with an increase in glucose and lactic acid contents and ADP/ATP ratio,whereas a decrease in insulin,5-HT,and DA levels was observed in the hippocampus.The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in hippocampal tissue decreased(P<0.05),and the synaptic ultrastructure of hippocampal neurons was damaged.Compared with the model group,depression-like behavioral changes,glucose metabolism,and monoamine neurotransmitter imbalance were alleviated in the CD300f agonist group and ZGF high-and low-dose group(P<0.05).The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in the hippocampus of the CD300f agonist group and the ZGF high-dose group were all increased(P<0.05),and synaptic damage was alleviated.The abnormal levels of glucose,lactate,ADP/ATP,5-HT,and CD300f protein expression were aggravated in the CD300f blocker group(P<0.05),and synaptic damage was aggravated.Conclusion ZGF can alleviate glucose metabolism disorders in hippocampal microglia and synaptic damage in hippocampal neurons in rats with diabetes-related depression.Its mechanism may be related to regulating the CD300f/GLUT1 signaling pathway.

Objective To explore the protective mechanism of Zuogui Jiangtang Jieyu Formula(ZGF)on synaptic damage of hippocampal neurons based on leukocyte mono-immunoglobulin-like receptor 3(CD300f)/glucose transporter 1(GLUT1)signal-mediated microglial glucose metabolism in rats with diabetes-related depression.Methods Eighty male SD rats were randomly selected using random number table method,with 10 rats serving as the normal group.The remaining 70 rats were fed a high-fat diet for 4 weeks and then injected once with 38 mg/kg of streptozotocin via the tail vein to replicate the diabetes rat model.Sixty rats were screened and successfully modeled,which were randomly divided into the model,CD300f blocker,CD300f agonist,metformin+fluoxetine(metformin 0.18 g/kg+fluoxetine 1.8 mg/kg),and ZGF high-and low-dose(20.52 and 10.26 g/kg,respectively)groups using random number table method.In addition to the normal group,the rats in the other groups underwent chronic unpredictable mild stress combined with isolation feeding for 28 days to replicate the diabetes-related depression rat model.The metformin+fluoxetine and ZGF high-and low-dose groups were subjected to continuous intragastrial administration for 14 days after the second week of modeling.The normal and model groups were administered an equal amount of distilled water by gavage.The CD300f blocker group and agonist group received microinjection into the hippocampus,with injection of myeloid cell trigger receptor inhibitory factor(CLM1,2 μg/kg)and immunoglobulin Fc surface protein(Fcγ,5 μg/kg)once a week,respectively.Depression-like behavior in rats was evaluated using open-field and forced swimming tests after the intervention.Biochemical analysis was used to detect the glucose,lactic acid,and adenosine diphosphate(ADP)/adenosine triphosphate(ATP)ratio contents.The insulin,5-hydroxytryptamine(5-HT),and dopamine(DA)levels in the hippocampus were detected using an enzyme-linked immunosorbent assay.Immunofluorescence was used to detect the average fluorescence intensity of CD300f,GLUT1,regulating synaptic membrane wxocytosis 3(RIMS3),and synapse-associated protein 102(SAP102)in hippocampal tissue.Western blotting was used to detect the CD300f,GLUT1,RIMS3,and SAP102 protein expression levels in the hippocampus.The synaptic damage of hippocampal neurons was observed using Nissl staining and transmission electron microscope.Results Compared with the normal group,the model group showed a decrease in the total active distance in the open-field test and an increase in forced swimming immobility time,with an increase in glucose and lactic acid contents and ADP/ATP ratio,whereas a decrease in insulin,5-HT,and DA levels was observed in the hippocampus.The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in hippocampal tissue decreased(P<0.05),and the synaptic ultrastructure of hippocampal neurons was damaged.Compared with the model group,depression-like behavioral changes,glucose metabolism,and monoamine neurotransmitter imbalance were alleviated in the CD300f agonist group and ZGF high-and low-dose group(P<0.05).The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in the hippocampus of the CD300f agonist group and the ZGF high-dose group were all increased(P<0.05),and synaptic damage was alleviated.The abnormal levels of glucose,lactate,ADP/ATP,5-HT,and CD300f protein expression were aggravated in the CD300f blocker group(P<0.05),and synaptic damage was aggravated.Conclusion ZGF can alleviate glucose metabolism disorders in hippocampal microglia and synaptic damage in hippocampal neurons in rats with diabetes-related depression.Its mechanism may be related to regulating the CD300f/GLUT1 signaling pathway.

Objective To explore the protective mechanism of Zuogui Jiangtang Jieyu Formula(ZGF)on synaptic damage of hippocampal neurons based on leukocyte mono-immunoglobulin-like receptor 3(CD300f)/glucose transporter 1(GLUT1)signal-mediated microglial glucose metabolism in rats with diabetes-related depression.Methods Eighty male SD rats were randomly selected using random number table method,with 10 rats serving as the normal group.The remaining 70 rats were fed a high-fat diet for 4 weeks and then injected once with 38 mg/kg of streptozotocin via the tail vein to replicate the diabetes rat model.Sixty rats were screened and successfully modeled,which were randomly divided into the model,CD300f blocker,CD300f agonist,metformin+fluoxetine(metformin 0.18 g/kg+fluoxetine 1.8 mg/kg),and ZGF high-and low-dose(20.52 and 10.26 g/kg,respectively)groups using random number table method.In addition to the normal group,the rats in the other groups underwent chronic unpredictable mild stress combined with isolation feeding for 28 days to replicate the diabetes-related depression rat model.The metformin+fluoxetine and ZGF high-and low-dose groups were subjected to continuous intragastrial administration for 14 days after the second week of modeling.The normal and model groups were administered an equal amount of distilled water by gavage.The CD300f blocker group and agonist group received microinjection into the hippocampus,with injection of myeloid cell trigger receptor inhibitory factor(CLM1,2 μg/kg)and immunoglobulin Fc surface protein(Fcγ,5 μg/kg)once a week,respectively.Depression-like behavior in rats was evaluated using open-field and forced swimming tests after the intervention.Biochemical analysis was used to detect the glucose,lactic acid,and adenosine diphosphate(ADP)/adenosine triphosphate(ATP)ratio contents.The insulin,5-hydroxytryptamine(5-HT),and dopamine(DA)levels in the hippocampus were detected using an enzyme-linked immunosorbent assay.Immunofluorescence was used to detect the average fluorescence intensity of CD300f,GLUT1,regulating synaptic membrane wxocytosis 3(RIMS3),and synapse-associated protein 102(SAP102)in hippocampal tissue.Western blotting was used to detect the CD300f,GLUT1,RIMS3,and SAP102 protein expression levels in the hippocampus.The synaptic damage of hippocampal neurons was observed using Nissl staining and transmission electron microscope.Results Compared with the normal group,the model group showed a decrease in the total active distance in the open-field test and an increase in forced swimming immobility time,with an increase in glucose and lactic acid contents and ADP/ATP ratio,whereas a decrease in insulin,5-HT,and DA levels was observed in the hippocampus.The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in hippocampal tissue decreased(P<0.05),and the synaptic ultrastructure of hippocampal neurons was damaged.Compared with the model group,depression-like behavioral changes,glucose metabolism,and monoamine neurotransmitter imbalance were alleviated in the CD300f agonist group and ZGF high-and low-dose group(P<0.05).The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in the hippocampus of the CD300f agonist group and the ZGF high-dose group were all increased(P<0.05),and synaptic damage was alleviated.The abnormal levels of glucose,lactate,ADP/ATP,5-HT,and CD300f protein expression were aggravated in the CD300f blocker group(P<0.05),and synaptic damage was aggravated.Conclusion ZGF can alleviate glucose metabolism disorders in hippocampal microglia and synaptic damage in hippocampal neurons in rats with diabetes-related depression.Its mechanism may be related to regulating the CD300f/GLUT1 signaling pathway.

Objective To explore the protective mechanism of Zuogui Jiangtang Jieyu Formula(ZGF)on synaptic damage of hippocampal neurons based on leukocyte mono-immunoglobulin-like receptor 3(CD300f)/glucose transporter 1(GLUT1)signal-mediated microglial glucose metabolism in rats with diabetes-related depression.Methods Eighty male SD rats were randomly selected using random number table method,with 10 rats serving as the normal group.The remaining 70 rats were fed a high-fat diet for 4 weeks and then injected once with 38 mg/kg of streptozotocin via the tail vein to replicate the diabetes rat model.Sixty rats were screened and successfully modeled,which were randomly divided into the model,CD300f blocker,CD300f agonist,metformin+fluoxetine(metformin 0.18 g/kg+fluoxetine 1.8 mg/kg),and ZGF high-and low-dose(20.52 and 10.26 g/kg,respectively)groups using random number table method.In addition to the normal group,the rats in the other groups underwent chronic unpredictable mild stress combined with isolation feeding for 28 days to replicate the diabetes-related depression rat model.The metformin+fluoxetine and ZGF high-and low-dose groups were subjected to continuous intragastrial administration for 14 days after the second week of modeling.The normal and model groups were administered an equal amount of distilled water by gavage.The CD300f blocker group and agonist group received microinjection into the hippocampus,with injection of myeloid cell trigger receptor inhibitory factor(CLM1,2 μg/kg)and immunoglobulin Fc surface protein(Fcγ,5 μg/kg)once a week,respectively.Depression-like behavior in rats was evaluated using open-field and forced swimming tests after the intervention.Biochemical analysis was used to detect the glucose,lactic acid,and adenosine diphosphate(ADP)/adenosine triphosphate(ATP)ratio contents.The insulin,5-hydroxytryptamine(5-HT),and dopamine(DA)levels in the hippocampus were detected using an enzyme-linked immunosorbent assay.Immunofluorescence was used to detect the average fluorescence intensity of CD300f,GLUT1,regulating synaptic membrane wxocytosis 3(RIMS3),and synapse-associated protein 102(SAP102)in hippocampal tissue.Western blotting was used to detect the CD300f,GLUT1,RIMS3,and SAP102 protein expression levels in the hippocampus.The synaptic damage of hippocampal neurons was observed using Nissl staining and transmission electron microscope.Results Compared with the normal group,the model group showed a decrease in the total active distance in the open-field test and an increase in forced swimming immobility time,with an increase in glucose and lactic acid contents and ADP/ATP ratio,whereas a decrease in insulin,5-HT,and DA levels was observed in the hippocampus.The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in hippocampal tissue decreased(P<0.05),and the synaptic ultrastructure of hippocampal neurons was damaged.Compared with the model group,depression-like behavioral changes,glucose metabolism,and monoamine neurotransmitter imbalance were alleviated in the CD300f agonist group and ZGF high-and low-dose group(P<0.05).The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in the hippocampus of the CD300f agonist group and the ZGF high-dose group were all increased(P<0.05),and synaptic damage was alleviated.The abnormal levels of glucose,lactate,ADP/ATP,5-HT,and CD300f protein expression were aggravated in the CD300f blocker group(P<0.05),and synaptic damage was aggravated.Conclusion ZGF can alleviate glucose metabolism disorders in hippocampal microglia and synaptic damage in hippocampal neurons in rats with diabetes-related depression.Its mechanism may be related to regulating the CD300f/GLUT1 signaling pathway.

Objective To explore the protective mechanism of Zuogui Jiangtang Jieyu Formula(ZGF)on synaptic damage of hippocampal neurons based on leukocyte mono-immunoglobulin-like receptor 3(CD300f)/glucose transporter 1(GLUT1)signal-mediated microglial glucose metabolism in rats with diabetes-related depression.Methods Eighty male SD rats were randomly selected using random number table method,with 10 rats serving as the normal group.The remaining 70 rats were fed a high-fat diet for 4 weeks and then injected once with 38 mg/kg of streptozotocin via the tail vein to replicate the diabetes rat model.Sixty rats were screened and successfully modeled,which were randomly divided into the model,CD300f blocker,CD300f agonist,metformin+fluoxetine(metformin 0.18 g/kg+fluoxetine 1.8 mg/kg),and ZGF high-and low-dose(20.52 and 10.26 g/kg,respectively)groups using random number table method.In addition to the normal group,the rats in the other groups underwent chronic unpredictable mild stress combined with isolation feeding for 28 days to replicate the diabetes-related depression rat model.The metformin+fluoxetine and ZGF high-and low-dose groups were subjected to continuous intragastrial administration for 14 days after the second week of modeling.The normal and model groups were administered an equal amount of distilled water by gavage.The CD300f blocker group and agonist group received microinjection into the hippocampus,with injection of myeloid cell trigger receptor inhibitory factor(CLM1,2 μg/kg)and immunoglobulin Fc surface protein(Fcγ,5 μg/kg)once a week,respectively.Depression-like behavior in rats was evaluated using open-field and forced swimming tests after the intervention.Biochemical analysis was used to detect the glucose,lactic acid,and adenosine diphosphate(ADP)/adenosine triphosphate(ATP)ratio contents.The insulin,5-hydroxytryptamine(5-HT),and dopamine(DA)levels in the hippocampus were detected using an enzyme-linked immunosorbent assay.Immunofluorescence was used to detect the average fluorescence intensity of CD300f,GLUT1,regulating synaptic membrane wxocytosis 3(RIMS3),and synapse-associated protein 102(SAP102)in hippocampal tissue.Western blotting was used to detect the CD300f,GLUT1,RIMS3,and SAP102 protein expression levels in the hippocampus.The synaptic damage of hippocampal neurons was observed using Nissl staining and transmission electron microscope.Results Compared with the normal group,the model group showed a decrease in the total active distance in the open-field test and an increase in forced swimming immobility time,with an increase in glucose and lactic acid contents and ADP/ATP ratio,whereas a decrease in insulin,5-HT,and DA levels was observed in the hippocampus.The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in hippocampal tissue decreased(P<0.05),and the synaptic ultrastructure of hippocampal neurons was damaged.Compared with the model group,depression-like behavioral changes,glucose metabolism,and monoamine neurotransmitter imbalance were alleviated in the CD300f agonist group and ZGF high-and low-dose group(P<0.05).The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in the hippocampus of the CD300f agonist group and the ZGF high-dose group were all increased(P<0.05),and synaptic damage was alleviated.The abnormal levels of glucose,lactate,ADP/ATP,5-HT,and CD300f protein expression were aggravated in the CD300f blocker group(P<0.05),and synaptic damage was aggravated.Conclusion ZGF can alleviate glucose metabolism disorders in hippocampal microglia and synaptic damage in hippocampal neurons in rats with diabetes-related depression.Its mechanism may be related to regulating the CD300f/GLUT1 signaling pathway.

Objective To explore the protective mechanism of Zuogui Jiangtang Jieyu Formula(ZGF)on synaptic damage of hippocampal neurons based on leukocyte mono-immunoglobulin-like receptor 3(CD300f)/glucose transporter 1(GLUT1)signal-mediated microglial glucose metabolism in rats with diabetes-related depression.Methods Eighty male SD rats were randomly selected using random number table method,with 10 rats serving as the normal group.The remaining 70 rats were fed a high-fat diet for 4 weeks and then injected once with 38 mg/kg of streptozotocin via the tail vein to replicate the diabetes rat model.Sixty rats were screened and successfully modeled,which were randomly divided into the model,CD300f blocker,CD300f agonist,metformin+fluoxetine(metformin 0.18 g/kg+fluoxetine 1.8 mg/kg),and ZGF high-and low-dose(20.52 and 10.26 g/kg,respectively)groups using random number table method.In addition to the normal group,the rats in the other groups underwent chronic unpredictable mild stress combined with isolation feeding for 28 days to replicate the diabetes-related depression rat model.The metformin+fluoxetine and ZGF high-and low-dose groups were subjected to continuous intragastrial administration for 14 days after the second week of modeling.The normal and model groups were administered an equal amount of distilled water by gavage.The CD300f blocker group and agonist group received microinjection into the hippocampus,with injection of myeloid cell trigger receptor inhibitory factor(CLM1,2 μg/kg)and immunoglobulin Fc surface protein(Fcγ,5 μg/kg)once a week,respectively.Depression-like behavior in rats was evaluated using open-field and forced swimming tests after the intervention.Biochemical analysis was used to detect the glucose,lactic acid,and adenosine diphosphate(ADP)/adenosine triphosphate(ATP)ratio contents.The insulin,5-hydroxytryptamine(5-HT),and dopamine(DA)levels in the hippocampus were detected using an enzyme-linked immunosorbent assay.Immunofluorescence was used to detect the average fluorescence intensity of CD300f,GLUT1,regulating synaptic membrane wxocytosis 3(RIMS3),and synapse-associated protein 102(SAP102)in hippocampal tissue.Western blotting was used to detect the CD300f,GLUT1,RIMS3,and SAP102 protein expression levels in the hippocampus.The synaptic damage of hippocampal neurons was observed using Nissl staining and transmission electron microscope.Results Compared with the normal group,the model group showed a decrease in the total active distance in the open-field test and an increase in forced swimming immobility time,with an increase in glucose and lactic acid contents and ADP/ATP ratio,whereas a decrease in insulin,5-HT,and DA levels was observed in the hippocampus.The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in hippocampal tissue decreased(P<0.05),and the synaptic ultrastructure of hippocampal neurons was damaged.Compared with the model group,depression-like behavioral changes,glucose metabolism,and monoamine neurotransmitter imbalance were alleviated in the CD300f agonist group and ZGF high-and low-dose group(P<0.05).The average fluorescence intensity and relative protein expression levels of CD300f,GLUT1,RIMS3,and SAP102 in the hippocampus of the CD300f agonist group and the ZGF high-dose group were all increased(P<0.05),and synaptic damage was alleviated.The abnormal levels of glucose,lactate,ADP/ATP,5-HT,and CD300f protein expression were aggravated in the CD300f blocker group(P<0.05),and synaptic damage was aggravated.Conclusion ZGF can alleviate glucose metabolism disorders in hippocampal microglia and synaptic damage in hippocampal neurons in rats with diabetes-related depression.Its mechanism may be related to regulating the CD300f/GLUT1 signaling pathway.