OBJECTIVE: To explore the feasibility and effectiveness of suture anchor double-pulley technique combined with suture three-dimensional binding via bone tunnel technique for avulsion fractures of the inferior pole of the patella. METHODS: A clinical data of 38 patients with avulsion fractures of the inferior pole of the patella, who met the selective criteria and were admitted between September 2021 and April 2023, was retrospectively analyzed. The fractures were treated with suture anchor double-pulley technique combined with suture three-dimensional binding via bone tunnel technique in 18 cases (group A) and steel wire tension-band fixation in 20 cases (group B). There was no significant difference in terms of age, gender, cause of fracture, side of fracture, and disease duration between the two groups ( P>0.05). The length of incision, operation time, occurrence of complications, the range of motion of knee joint, and Böstman score of knee joint at last follow-up were recorded. The fracture healing was evaluated through X-ray films and the time of fracture healing was recorded. RESULTS: All incisions healed by first intention. The length of incision was significantly shorter in group A than in group B ( P<0.05). There was no significant difference in the operation time between the two groups ( P>0.05). All patients were followed up 12-24 months (mean, 16.1 months). X-ray films showed that all fractures healed and there was no significant difference in the healing time between the two groups ( P>0.05). At last follow-up, the range of motion and Böstman score of the knee joint in group A were significantly better than those in group B ( P<0.05). During follow-up, 1 patient (5.6%) in group A had one anchor mild prolapse and 3 patients (15.0%) occured internal fixation irritation in group B. But there was no significant difference in the incidence of complications between the two groups ( P>0.05). CONCLUSION For the avulsion fractures of the inferior pole of the patella, the suture anchor double-pulley technique combined with suture three-dimensional binding via bone tunnel technique has advantages of reliable fixation, small incision, avoidance of secondary operation to remove internal fixator, and fewer complications, with definite effectiveness.
Humans ; Male ; Female ; Patella/surgery* ; Suture Anchors ; Fracture Fixation, Internal/instrumentation* ; Adult ; Retrospective Studies ; Middle Aged ; Fractures, Avulsion/surgery* ; Treatment Outcome ; Young Adult ; Range of Motion, Articular ; Fracture Healing ; Adolescent ; Suture Techniques ; Knee Joint/physiopathology*

Objective:To investigate the prognosis of patients with initially resectable gastric cancer liver metastasis (GCLM) who were treated by different modalities, and analyze the influencing factors for prognosis of patients.Methods:The retrospective cohort study was conducted. The clinicopathological data of 327 patients with initially resectable GCLM who were included in the database of a nationwide multicenter retrospective cohort study on GCLM based on real-world data from January 2010 to December 2019 were collected. There were 267 males and 60 females, aged 61(54,68)years. According to the specific situations of patients, treatment modalities included radical surgery combined with systemic treatment, palliative surgery combined with systemic treatment, and systemic treatment alone. Observation indicators: (1) clinical characteristics of patients who were treated by different modalities; (2) prognostic outcomes of patients who were treated by different modalities; (3) analysis of influencing factors for prognosis of patients with initially resectable GCLM; (4) screening of potential beneficiaries in patients who were treated by radical surgery plus systemic treatment and patients who were treated by palliative surgery plus systemic treatment. Measurement data with normal distribution were represented as Mean± SD, and comparison between groups was conducted using the independent sample t test. Measurement data with skewed distribution were represented as M( Q1, Q3), and comparison between groups was conducted using the rank sum test. Count data were described as absolute numbers or percentages, and comparison between groups was conducted using the chi-square test. The Kaplan-Meier method was used to calculate survival rate and draw survival curve, and Log-Rank test was used for survival analysis. Univariate and multivariate analyses were conducted using the COX proportional hazard regression model. The propensity score matching was employed by the 1:1 nearest neighbor matching method with a caliper value of 0.1. The forest plots were utilized to evaluate potential benefits of diverse surgical combined with systemic treatments within the population. Results:(1) Clinical characteristics of patients who were treated by different modalities. Of 327 patients, there were 118 cases undergoing radical surgery plus systemic treatment, 164 cases undergoing palliative surgery plus systemic treatment, and 45 cases undergoing systemic treatment alone. There were significant differences in smoking, drinking, site of primary gastric tumor, diameter of primary gastric tumor, site of liver metastasis, and metastatic interval among the three groups of patients ( P<0.05). (2) Prognostic outcomes of patients who were treated by different modalities. The median overall survival time of the 327 pati-ents was 19.9 months (95% confidence interval as 14.9-24.9 months), with 1-, 3-year overall survival rate of 61.3%, 32.7%, respectively. The 1-year overall survival rates of patients undergoing radical surgery plus systemic treatment, palliative surgery plus systemic treatment and systemic treatment alone were 68.3%, 63.1%, 30.6%, and the 3-year overall survival rates were 41.1%, 29.9%, 11.9%, showing a significant difference in overall survival rate among the three groups of patients ( χ2=19.46, P<0.05). Results of further analysis showed that there was a significant difference in overall survival rate between patients undergoing radical surgery plus systemic treatment and patients undergoing systemic treatment alone ( hazard ratio=0.40, 95% confidence interval as 0.26-0.61, P<0.05), between patients undergoing palliative surgery plus systemic treatment and patients under-going systemic treatment alone ( hazard ratio=0.47, 95% confidence interval as 0.32-0.71, P<0.05). (3) Analysis of influencing factors for prognosis of patients with initially resectable GCLM. Results of multivariate analysis showed that the larger primary gastric tumor, poorly differentiated tumor, larger liver metastasis, multiple hepatic metastases were independent risk factors for prognosis of patients with initially resectable GCLM ( hazard ratio=1.20, 1.70, 1.20, 2.06, 95% confidence interval as 1.14-1.27, 1.25-2.31, 1.04-1.42, 1.45-2.92, P<0.05) and immunotherapy or targeted therapy, the treatment modality of radical or palliative surgery plus systemic therapy were independent protective factors for prognosis of patients with initially resectable GCLM ( hazard ratio=0.60, 0.39, 0.46, 95% confidence interval as 0.42-0.87, 0.25-0.60, 0.30-0.70, P<0.05). (4) Screening of potentinal beneficiaries in patients who were treated by radical surgery plus systemic treatment and patients who were treated by palliative surgery plus systemic treatment. Results of forest plots analysis showed that for patients with high-moderate differentiated GCLM and patients with liver metastasis located in the left liver, the overall survival rate of patients undergoing radical surgery plus systemic treatment was better than patients undergoing palliative surgery plus systemic treatment ( hazard ratio=0.21, 0.42, 95% confidence interval as 0.09-0.48, 0.23-0.78, P<0.05). Conclusions:Compared to systemic therapy alone, both radical and palliative surgery plus systemic therapy can improve the pro-gnosis of patients with initially resectable GCLM. The larger primary gastric tumor, poorly differen-tiated tumor, larger liver metastasis, multiple hepatic metastases are independent risk factors for prognosis of patients with initial resectable GCLM and immunotherapy or targeted therapy, the treatment modality of radical or palliative surgery plus systemic therapy are independent protective factors for prognosis of patients with initially resectable GCLM.

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.

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.