Objective: To address systemic challenges in the blood system, such as supply-demand imbalance, inefficient allocation, and inappropriate clinical use, while bridging gaps in current theories regarding the integration of social mobilization, institutional practice, and policy coordination. It sought to construct a system dynamics model spanning from macro to micro levels to analyze the blood management system holistically. Methods: Key variables were identified by a systematic literature search in both Chinese and English databases. An improved Delphi method was then employed to conduct expert consultations across different fields, leading to the selection and determination of core variable sets for each sub-model. Furthermore, by defining their logical relationships, a system dynamics model was constructed to systematically analyze the operation mechanism of the blood management system. Results: Four core sub-models were developed: 1) A macro "Dynamic Balance" model quantifying regional supply-demand equilibrium and inventory control; 2) a mobilization "Three-Layer Funnel" model analyzing how socio-cultural factors, service channels, and policy incentives influence donation behavior; 3) an institutional "Dual-Cycle Regulation" model revealing hospital blood usage is driven by both disease burden (demand cycle) and management practices (regulation cycle); and 4) an individual "Three-Layer Filter" model standardizing clinical transfusion decisions based on necessity, risk-benefit, and context. These were integrated into a "Multi-Layer Linkage and Feedback" model, elucidating bidirectional interactions among five levels: policy environment, regional supply, blood station mobilization, hospital application, and clinical decision-making. Conclusion: This study constructed a system dynamics model for blood management. By defining key variables and their logical relationships, it systematically analyzes the system′s operational mechanism. The integrated framework connects multiple levels—regional supply, voluntary donation, hospital blood use, and clinical decision-making—revealing their intrinsic linkages. Future efforts should employ systems thinking to synergistically enhance supply-side mobilization, demand-side management, systemic regulation, and decision standardization to build a safe, efficient, and sustainable blood security system.

ObjectiveTo investigate the mechanism of Shenkang injection in delaying diabetic kidney disease by regulating endoplasmic reticulum stress and attenuating podocyte apoptosis through the Glucose regulated protein 78 （ GRP78 ） / transcription factor C / EBP homologous protein （ CHOP ） signaling pathway （GRP78/CHOP） signaling pathway. MethodsFor the animal experiment， 10 12-week-old db/m mice were selected as a normal group， and 30 12-week-old db/db mice were randomly divided into a model group， a Shenkang injection group （15.6 mL·kg^-1）， and a dapagliflozin group （1.6 mg·kg^-1）. To observe the general condition of mice， fasting blood glucose， urinary albumin/urine creatinine （ACR）， and 24 h urine protein quantification were detected in each group before drug administration. After 12 weeks of drug treatment， mice were tested for fasting blood glucose， total cholesterol （TC）， triglyceride （TG）， low-density cholesterol （LDL）， ACR， 24 h urine protein quantification， blood creatinine （SCr）， and blood urea （UREA）. Hematoxylin-eosin （HE） staining， periodic acid-Schiff （PAS） staining， and transmission electron microscopy were used to observe the pathologic morphology in renal tissue. Immunohistochemistry was used to detect the expressions of nephroprotective marker protein （Nephrin）， glucose-regulated protein 78 （GRP78）， CCAAT/enhancer-binding protein homologous protein （CHOP）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in renal tissue. Western blot was used to detect the expressions of GRP78， CHOP， Bcl-2， Bax， and Nephrin proteins， and Real-time polymerase chain reaction （Real-time PCR） was employed to detect the expressions of Nephrin， GRP78， CHOP， Bcl-2， and Bax mRNAs in renal tissue. ResultsBefore drug administration， compared with those in the normal group， the body mass of db/db mice was significantly increased， and blood glucose， 24 h urine protein quantification， and ACR were significantly elevated in the Shenkang injection group and Dapagliflozin group （P<0.01）. After 12 weeks of administration， compared with those in the model group， the general state of mice in the Shenkang injection group was significantly improved， and the body mass was decreased. The blood glucose was significantly reduced （P<0.01）， and blood lipids TC， TG， and LDL were significantly decreased （P<0.05， P<0.01）. The 24 h urine protein quantification and ACR were significantly decreased （P<0.05）， and SCr and UREA were significantly reduced （P<0.01）. Compared with those of the model group， the pathologic results of the Shenkang injection group showed that proliferation of mesangial cells， reduction of inflammatory cell infiltration， and alleviation of renal tubular vacuolization and podocyte damage were observed in renal tissue of mice. Electron microscopy showed that fusion of the pedicle protruding and thickening of the basement membrane were reduced. Immunohistochemistry results showed that the expressions of GRP78， CHOP， and Bax proteins were significantly reduced （P<0.01）， and the expressions of Nephrin and Bcl-2 proteins were significantly increased （P<0.01） in renal tissue of the Shenkang injection group. Western blot results showed that the expressions of Nephrin and Bcl-2 in the Shenkang injection group were significantly increased （P<0.05， P<0.01）， and the expressions of GRP78， CHOP， and Bax proteins were significantly decreased （P<0.05， P<0.01）. Real-time PCR results showed that the expressions of GRP78， CHOP， and Bax mRNAs were down regulated in the Shenkang injection group （P<0.01）， and the expressions of Nephrin and Bcl-2 mRNAs were up regulated （P<0.01）. ConclusionShenkang injection inhibits endoplasmic reticulum stress response and podocyte apoptosis by regulating the GRP78/CHOP signaling pathway， which in turn ensures the integrity of glomerular filtration barrier， reduces the occurrence of proteinuria， improves renal function， and thus delays the progression of diabetic kidney disease.

ObjectiveTo investigate the mechanism of Shenkang injection in delaying diabetic kidney disease by regulating endoplasmic reticulum stress and attenuating podocyte apoptosis through the Glucose regulated protein 78 （ GRP78 ） / transcription factor C / EBP homologous protein （ CHOP ） signaling pathway （GRP78/CHOP） signaling pathway. MethodsFor the animal experiment， 10 12-week-old db/m mice were selected as a normal group， and 30 12-week-old db/db mice were randomly divided into a model group， a Shenkang injection group （15.6 mL·kg^-1）， and a dapagliflozin group （1.6 mg·kg^-1）. To observe the general condition of mice， fasting blood glucose， urinary albumin/urine creatinine （ACR）， and 24 h urine protein quantification were detected in each group before drug administration. After 12 weeks of drug treatment， mice were tested for fasting blood glucose， total cholesterol （TC）， triglyceride （TG）， low-density cholesterol （LDL）， ACR， 24 h urine protein quantification， blood creatinine （SCr）， and blood urea （UREA）. Hematoxylin-eosin （HE） staining， periodic acid-Schiff （PAS） staining， and transmission electron microscopy were used to observe the pathologic morphology in renal tissue. Immunohistochemistry was used to detect the expressions of nephroprotective marker protein （Nephrin）， glucose-regulated protein 78 （GRP78）， CCAAT/enhancer-binding protein homologous protein （CHOP）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in renal tissue. Western blot was used to detect the expressions of GRP78， CHOP， Bcl-2， Bax， and Nephrin proteins， and Real-time polymerase chain reaction （Real-time PCR） was employed to detect the expressions of Nephrin， GRP78， CHOP， Bcl-2， and Bax mRNAs in renal tissue. ResultsBefore drug administration， compared with those in the normal group， the body mass of db/db mice was significantly increased， and blood glucose， 24 h urine protein quantification， and ACR were significantly elevated in the Shenkang injection group and Dapagliflozin group （P<0.01）. After 12 weeks of administration， compared with those in the model group， the general state of mice in the Shenkang injection group was significantly improved， and the body mass was decreased. The blood glucose was significantly reduced （P<0.01）， and blood lipids TC， TG， and LDL were significantly decreased （P<0.05， P<0.01）. The 24 h urine protein quantification and ACR were significantly decreased （P<0.05）， and SCr and UREA were significantly reduced （P<0.01）. Compared with those of the model group， the pathologic results of the Shenkang injection group showed that proliferation of mesangial cells， reduction of inflammatory cell infiltration， and alleviation of renal tubular vacuolization and podocyte damage were observed in renal tissue of mice. Electron microscopy showed that fusion of the pedicle protruding and thickening of the basement membrane were reduced. Immunohistochemistry results showed that the expressions of GRP78， CHOP， and Bax proteins were significantly reduced （P<0.01）， and the expressions of Nephrin and Bcl-2 proteins were significantly increased （P<0.01） in renal tissue of the Shenkang injection group. Western blot results showed that the expressions of Nephrin and Bcl-2 in the Shenkang injection group were significantly increased （P<0.05， P<0.01）， and the expressions of GRP78， CHOP， and Bax proteins were significantly decreased （P<0.05， P<0.01）. Real-time PCR results showed that the expressions of GRP78， CHOP， and Bax mRNAs were down regulated in the Shenkang injection group （P<0.01）， and the expressions of Nephrin and Bcl-2 mRNAs were up regulated （P<0.01）. ConclusionShenkang injection inhibits endoplasmic reticulum stress response and podocyte apoptosis by regulating the GRP78/CHOP signaling pathway， which in turn ensures the integrity of glomerular filtration barrier， reduces the occurrence of proteinuria， improves renal function， and thus delays the progression of diabetic kidney disease.

Objective To investigate the effects of neurotrophic factor Neuritin overexpression on the angiogenic effects of chicken embryonic allantoic membrane (CAM) and human umbilical vein endothelial cells (HUVECs),and to provide a new direction for the treatment of angiogenic diseases. Methods Thirty fresh yellow-skinned breeding eggs were selected to establish a CAM model,which were divided into three groups by randomized numerical table method:positive control group (bFGF),negative control group (NS) and experimental group (Neuritin),with 10 eggs in each group. The positive control group was loaded with 2500 U/mL of bFGF,the experimental group was loaded with 10 μg/mL of Neuritin protein,and the negative control group was loaded with NS. 10 μL loading volume was loaded into each group,and all CAMs were incubated at the same temperature,relative humidity,and time,and the vascular branching,number,and size of the CAMs in each group were recorded after 72 h of incubation. Fresh umbilical cords from healthy pregnant women were selected to produce primary HUVECs,which were divided into three groups:transfected with recombinant plasmid (HUVEC-neu group),transfected with empty vector (HUVEC-3.1 group),and untransfected (HUVEC group). Primary HUVECs in the HUVEC-neu group were transfected with the recombinant plasmid Neuritin,and those in the HUVEC-3.1 group were transfected with the empty vector. HUVEC-3.1 group was transfected with the empty vector plasmid,and HUVEC group was not given any special treatment,and all three groups received the same culture regimen. Western blot was used to detect the protein expression level of Neuritin in HUVEC-3.1 and HUVEC-neu groups. CCK-8 assay,cell scratch assay,Transwell assay,and tube formation assay were used to detect protein expression level of Neuritin in HUVEC-3.1 group and HUVEC-neu group,and HUVEC-neu groups for cell proliferation,migration and tube formation. Results (1) The number of CAM vessel branch points and microvessels in the experimental group was significantly increased compared with that in the negative control group (P<0.01),but there was no statistically significant difference in the number of large and medium-sized vessels between the two groups (P>0.05);(2) Neuritin was successfully overexpressed in HUVECs in the HUVEC-neu group. (3) Compared with the HUVEC-3.1 group,the proliferation vigor of cells in the HUVEC-neu group was decreased (P<0.05),but their migration and tube formation abilities were significantly enhanced (P<0.01). Conclusion Neuritin overexpression promotes angiogenesis and participates in the regulation of neovascularization by affecting cell prolif-eration,migration,and tube formation ability.

Objective:To explore the influencing of 18F-fluorodeoxyglucose positron emission tomography/computed tomography ( 18F-FDG PET/CT) indicators on microvascular invasion (MVI) of hepatocellular carcinoma and to construct a nomogram for predicting MVI. Methods:The data of 125 patients with hepatocellular carcinoma who underwent 18F-FDG PET/CT from January 2012 to March 2024 in the Second Xiangya Hospital of Central South University were retrospectively collected and analyzed. There were 108 males and 17 females, with the age of (51.8±7.6) years. The 125 patients were divided into MVI negative group ( n=51) and MVI positive group ( n=74) according to whether MVI was positive. The two groups were compared in terms of liver cirrhosis, aspartate transaminase (AST), γ-glutamyltransferase, carbohydrate antigen 125, Ki-67, maximum tumor diameter, tumor capsule, combined portal vein tumor thrombus, and 18F-FDG PET/CT indicators maximum standard uptake value (SUVmax), tumor metabolic volume, total glycolysis of lesions, tumor-liver ratio (TLR), and tumor-mediastinum ratio. Multivariate logistic regression was used to analyze the influencing factors of MVI, and a nomogram MVI prediction model was constructed. Results:Cirrhosis, AST >40 U/L, γ-glutamyltransferase >60 U/L, carbohydrate antigen 125>35 U/ml, Ki-67 >20%, maximum tumor diameter, tumor capsule, combined portal vein tumor thrombus, SUVmax >6.30, tumor metabolic volume >45.48, total glycolysis of lesions >253.22, TLR >2.39, tumor-mediastinum ratio >4.27 were associated with MVI in patients with hepatocellular carcinoma (all P<0.05). Multivariate logistic regression analysis showed that combined portal vein tumor thrombus ( OR=40.244, 95% CI: 5.276-306.986), SUVmax >6.30 ( OR=3.920, 95% CI: 1.841-8.346), tumor metabolic volume>45.48 ( OR=6.482, 95% CI: 2.914-14.415), TLR>2.39 ( OR=7.250, 95% CI: 3.247-16.188) were influencing factors of MVI in patients with hepatocellular carcinoma (all P<0.05). A nomogram for predicting MVI was constructed based on the multivariate results. Conclusion:18F-FDG PET/CT index SUVmax, tumor metabolic volume, and TLR are influencing factors for MVI of hepatocellular carcinoma patients. Based on these influencing factors, a nomogram model for predicting MVI can be constructed.

Objective To investigate the differences of cerebral vascular morphology and serum indexes between patients with vascular cognitive impairment no dementia(VCIND)and cognitively normal cerebral vascular disease.Methods A total of 100 VCIND patients hospitalized in Quzhou Hospital of Zhejiang Medical and Health Group from June 2023 to September 2024 were included in experimental group,and 100 cognitively normal patients with cerebral vascular disease hospitalized during the same period were included in control group.Cerebral artery extension and dilation,cerebrovascular stenosis,collateral circulation establishment,inflammatory factors and lipid metabolism indexes were compared between two groups by means of cerebrovascular angiography and serum examination.The relationship between the severity of cognitive impairment and the vascular lesion of different responsibility was also explored.Results The rate of cerebral artery extension and dilation,rate of vascular stenosis in experimental group were higher than those in control group,and the rate of collateral circulation establishment was lower than that in control group(P＜0.05).The levels of interleukin-6,interleukin-1 β,tumor necrosis factor-α,total cholesterol,low density lipoprotein,apolipoprotein B and lipoprotein(a)in experimental group were significantly higher than those in control group,level of high density lipoprotein was lower than that in control group(P＜0.05).In experimental group,there were 20 cases of anterior cerebral artery vascular disease,22 cases of middle cerebral artery vascular disease,26 cases of posterior cerebral artery vascular disease,32 cases of vertebrobasilar artery vascular disease.There were no significant differences in the scores of mini-mental state examination,Montreal cognitive assessment and Hachinski ischemic scale among patients with different responsible vascular diseases(P＞0.05).Conclusion Patients with cerebral artery extension and dilation,cerebral artery stenosis,no establishment of collateral circulation,inflammatory response and abnormal lipid metabolism were high-risk groups for VCIND.Such patients need early cognitive intervention to prevent VCIND occurrence.

Objective:To explore the correlation between nurses' electronic health literacy and their health education competence.Methods:A convenience sampling method was used to select nurses from 24 secondary and tertiary hospitals in Jincheng for the study from July to August 2022. The Mobile-e Health Literacy Scale and the Nurse Health Education Competence Self-assessment Scale were used to survey the subjects. Pearson correlation analysis was performed to analyze the correlation between nurses' electronic health literacy and their health education competence. Canonical correlation analysis was employed to build a standardized canonical correlation model, conduct canonical structure analysis, and canonical redundancy analysis to explore the relationship between electronic health literacy and health education competence in nurses.Results:A total of 705 questionnaires were distributed, 74 were excluded due to short response times (<120 seconds), regular responses, or incorrect fillings, leaving 631 valid questionnaires, with an effective response rate of 89.5%. The total score of the Mobile-e Health Literacy Scale for 631 nurses was (50.40±8.75), with scores of (12.69±2.41) for self-perception, (21.35±3.70) for information acquisition, and (16.36±3.29) for interaction judgment. The total score for the Nurse Health Education Competence Self-assessment Scale was (366.32±57.51), with subscale scores of (29.71±4.77) for knowledge and experience, (95.65±14.20) for comprehensive quality, and (240.97±40.85) for skills and abilities. The total score of electronic health literacy and the scores of each dimension were positively correlated with the scores of each subscale of health education competence ( P<0.01). Canonical correlation analysis identified three pairs of canonical variables, with correlation coefficients of 0.750, 0.279, and 0.067 for the first, second, and third pairs, respectively. The correlation coefficients of the first and second pairs were statistically significant ( P<0.01). Nurses' electronic health literacy was primarily determined by interaction judgment ( r=-0.982), while health education competence was primarily determined by skills and abilities ( r=-0.995) . Conclusions:There is a positive correlation between nurses' electronic health literacy and health education competence. Enhancing nurses' electronic health literacy is of significant importance for improving their health education competence.

Objective:To investigate the application value of 68Ga-Pentixafor PET/CT targeting CXC subfamily receptor 4 (CXCR4) in the subtyping and precise localization of primary aldosteronism (PA). Methods:Thirty-three patients with PA confirmed by clinical examination and undergoing 68Ga-Pentixafor PET/CT and adrenal vein sampling (AVS) in the Second Xiangya Hospital between July 1st 2022 and July 1st 2023 were prospectively enrolled (24 males, 9 females, age (49.6±10.3) years). Patients with a dominant side identified by PET/CT or AVS underwent unilateral adrenalectomy, while those without a dominant side received medical treatment. According to the standard of PA surgical outcome (PASO), patients underwent surgery were divided into unilateral PA (UPA) and bilateral PA (BPA) based on the pathological and follow-up results. Those who received medical treatment were BPA. The diagnostic efficacy of 68Ga-Pentixafor PET/CT for UPA was calculated. The ROC curve was constructed to analyze the accuracy and optimal threshold of SUV max, the ratio of lesion SUV max to contralateral adrenal tissue SUV mean (LCR), and the ratio of lesion SUV max to liver SUV mean (LLR) in the diagnosis of PA subtype. The correlation between the quantitative parameters and the clinical features and lesion width of the patients was evaluated by Spearman rank correlation analysis. The differences of LCR and LLR between different efficacy groups were compared by the independent-sample t test. Results:A total of 20 patients underwent unilateral adrenalectomy. Nineteen patients were finally diagnosed with UPA and 14 with BPA. The agreement rate of PET/CT and AVS was 81.8%(27/33), and both methods independently detected UPA that was negative in the other examination. The sensitivity, specificity, and accuracy of 68Ga-Pentixafor PET/CT visual diagnosis of UPA were 18/19, 14/14, and 97.0%(32/33), respectively. ROC curve showed that the AUC of LLR for subtype diagnosis was 0.944, with the optimal threshold of 3.1. SUV max, LCR, and LLR were positively correlated with aldosterone concentration ( rs values: 0.35, 0.47, and 0.36, all P<0.05) and lesion width ( rs values: 0.43, 0.49, and 0.58, all P<0.05). The LCR (3.9±2.2 vs 1.6±0.3; t=2.00, P=0.041) and LLR( 8.7±4.1 vs 4.2±1.3; t=2.06, P=0.045) of the dominant side lesions in patients who achieved complete biochemical and clinical cure were higher than those in patients with partial improvement. Conclusions:68Ga-Pentixafor PET/CT imaging can be used in the diagnosis and precise localization of PA subtype. It also can detect patients with PA which can be surgically cured but not detected by AVS, and the quantitative analysis may be valuable for prognosis prediction.

Objective To investigate the effects of neurotrophic factor Neuritin overexpression on the angiogenic effects of chicken embryonic allantoic membrane (CAM) and human umbilical vein endothelial cells (HUVECs),and to provide a new direction for the treatment of angiogenic diseases. Methods Thirty fresh yellow-skinned breeding eggs were selected to establish a CAM model,which were divided into three groups by randomized numerical table method:positive control group (bFGF),negative control group (NS) and experimental group (Neuritin),with 10 eggs in each group. The positive control group was loaded with 2500 U/mL of bFGF,the experimental group was loaded with 10 μg/mL of Neuritin protein,and the negative control group was loaded with NS. 10 μL loading volume was loaded into each group,and all CAMs were incubated at the same temperature,relative humidity,and time,and the vascular branching,number,and size of the CAMs in each group were recorded after 72 h of incubation. Fresh umbilical cords from healthy pregnant women were selected to produce primary HUVECs,which were divided into three groups:transfected with recombinant plasmid (HUVEC-neu group),transfected with empty vector (HUVEC-3.1 group),and untransfected (HUVEC group). Primary HUVECs in the HUVEC-neu group were transfected with the recombinant plasmid Neuritin,and those in the HUVEC-3.1 group were transfected with the empty vector. HUVEC-3.1 group was transfected with the empty vector plasmid,and HUVEC group was not given any special treatment,and all three groups received the same culture regimen. Western blot was used to detect the protein expression level of Neuritin in HUVEC-3.1 and HUVEC-neu groups. CCK-8 assay,cell scratch assay,Transwell assay,and tube formation assay were used to detect protein expression level of Neuritin in HUVEC-3.1 group and HUVEC-neu group,and HUVEC-neu groups for cell proliferation,migration and tube formation. Results (1) The number of CAM vessel branch points and microvessels in the experimental group was significantly increased compared with that in the negative control group (P<0.01),but there was no statistically significant difference in the number of large and medium-sized vessels between the two groups (P>0.05);(2) Neuritin was successfully overexpressed in HUVECs in the HUVEC-neu group. (3) Compared with the HUVEC-3.1 group,the proliferation vigor of cells in the HUVEC-neu group was decreased (P<0.05),but their migration and tube formation abilities were significantly enhanced (P<0.01). Conclusion Neuritin overexpression promotes angiogenesis and participates in the regulation of neovascularization by affecting cell prolif-eration,migration,and tube formation ability.

ObjectiveTo explore the mechanism of Yishen Huashi granules in alleviating renal tubular epithelial cell injury and relieving diabetic kidney disease by regulating the mitogen-activated protein kinase （MAPK） signaling pathway. MethodsThe db/db mice of 12 weeks old were randomly assigned into model ， dapagliflozin （1.6 mg·kg^-1）， and Yishen Huashi granules （4.7 g·kg^-1）， and db/m mice were used as the control group. The general conditions of mice were observed， and fasting blood glucose and 24-h urinary protein and albumin-to-creatinine ratio （ACR） were measured at weeks 0 and 12 of administration. After 12 weeks of treatment， the levels of serum creatinine （SCr）， blood urea （UREA）， triglycerides （TG）， total cholesterol （TC）， and low density lipoprotein （LDL） were measured. The pathological changes in the renal tissue were observed by hematoxylin-eosin （HE） staining， Periodic acid-Schiff （PAS） staining， Mallory staining， and transmission electron microscopy. Real-time PCR was employed to determine the mRNA levels of monocyte chemotactic protein-1 （MCP-1） and CC chemokine receptor-2 （CCR2） in the renal tissue of mice. The immunohistochemical assay was employed to examine the expression of p38， phospho-p38 （p-p38）， MCP-1， and CCR2 in the renal tissue of mice. Western blotting was employed to measure the protein levels of p-p38， p38， MCP-1， and CCR2 in the renal tissue of mice.HK-2 cells cultured in vitro were grouped as follows： negative control， high glucose（30 mmol·L^-1）， Yishen Huashi granule-containing serum， and SB203580. After 48 h of cell culture in each group， RNA were extracted and the levels of MCP-1， and CCR2 mRNA were determined by Real-time PCR，proteins were extracted and the levels of p38， p-p38， MCP-1， and CCR2 were determined by Western blot. ResultsThe in vivo experiments showed that before treatment， other groups had higher body weight， blood glucose level， 24 h urinary protein， and ACR than the control group （P<0.05，P<0.01）. After 12 weeks of treatment， compared with the model group， the Yishen Huashi granules group showed improved general conditions， a decreasing trend in body weight， lowered levels of blood glucose， 24-h urinary protein， and ACR （P<0.01）， reduced SCr and UREA （P<0.01）， and declined levels of TC， TG， and LDL （P<0.05，P<0.01）. Compared with the model group， the Yishen Huashi granules group showed alleviated damage and interstitial fibrosis in the renal tissue as well as reductions in glomerular foot process fusion and basement membrane thickening. Moreover， the Yishen Huashi granules group showed down-regulated mRNA levels of MCP-1 and CCR2 （P<0.01）， reduced positive expression of p-p38， MCP-1， and CCR2 （P<0.01）， and down-regulated protein levels of p-p38/p38， MCP-1， and CCR2 （P<0.05） in the renal tissue. The cell experiment showed that compared with the high glucose group， the Yishen Huashi granule-containing serum group showcased down-regulated mRNA levels of MCP-1 and CCR2 （P<0.01） and down-regulated protein levels of p-p38/p38， MCP-1， and CCR2（P<0.05，P<0.01）. ConclusionYishen Huashi granules can regulate glucose-lipid metabolism， reduce 24 h urinary protein and ACR， improve the renal function， alleviate the renal tubule injury caused by high glucose， and protect renal tubule epithelial cells in db/db mice by reducing MCP-1/CCR2 activation via the p38 MAPK signaling pathway.