BACKGROUND:Osteosarcoma has a complex pathogenesis and a poor prognosis.While advancements in medical technology have led to some improvements in the 5-year survival rate,substantial progress in its treatment has not yet been achieved. OBJECTIVE:To screen key molecular markers in osteosarcoma,analyze their relationship with osteosarcoma treatment drugs,and explore the potential disease mechanisms of osteosarcoma at the molecular level. METHODS:GSE99671 and GSE284259(miRNA)datasets were obtained from the Gene Expression Omnibus database.Differential gene expression analysis and Weighted Gene Co-expression Network Analysis(WGCNA)on GSE99671 were performed.Functional enrichment analysis was conducted using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes separately for the differentially expressed genes and the module genes with the highest positive correlation to the disease.The intersection of these module genes and differentially expressed genes was taken as key genes.A Protein-Protein Interaction network was constructed,and correlation analysis on the key genes was performed using CytoScape software,and hub genes were identified.Hub genes were externally validated using the GSE28425 dataset and text validation was conducted.The drug sensitivity of hub genes was analyzed using the CellMiner database,with a threshold of absolute value of correlation coefficient|R|>0.3 and P<0.05. RESULTS AND CONCLUSION:(1)Differential gene expression analysis identified 529 differentially expressed genes,comprising 177 upregulated and 352 downregulated genes.WGCNA analysis yielded a total of 592 genes with the highest correlation to osteosarcoma.(2)Gene Ontology enrichment results indicated that the development of osteosarcoma may be associated with extracellular matrix,bone cell differentiation and development,human immune regulation,and collagen synthesis and degradation.Kyoto Encyclopedia of Genes and Genomes enrichment results showed the involvement of pathways such as PI3K-Akt signaling pathway,focal adhesion signaling pathway,and immune response in the onset of osteosarcoma.(3)The intersection analysis revealed a total of 59 key genes.Through Protein-Protein Interaction network analysis,8 hub genes were selected,which were LUM,PLOD1,PLOD2,MMP14,COL11A1,THBS2,LEPRE1,and TGFB1,all of which were upregulated.(4)External validation revealed significantly downregulated miRNAs that regulate the hub genes,with hsa-miR-144-3p and hsa-miR-150-5p showing the most significant downregulation.Text validation results demonstrated that the expression of hub genes was consistent with previous research.(5)Drug sensitivity analysis indicated a negative correlation between the activity of methotrexate,6-mercaptopurine,and pazopanib with the mRNA expression of PLOD1,PLOD2,and MMP14.Moreover,zoledronic acid and lapatinib showed a positive correlation with the mRNA expression of PLOD1,LUM,MMP14,PLOD2,and TGFB1.This suggests that zoledronic acid and lapatinib may be potential therapeutic drugs for osteosarcoma,but further validation is required through additional basic experiments and clinical studies.

BACKGROUND:Chondrocyte apoptosis is an important factor in the development of osteoarthritis,and Complanatoside A has a flavonoid effect,which can inhibit apoptosis of various cells,but its effect on chondrocyte apoptosis and the mechanism of action are not clear. OBJECTIVE:To investigate the intrinsic association and mechanism of Complanatoside A in chondrocyte apoptosis based on the Wnt/β-catenin signaling pathway. METHODS:(1)The cartilage tissues of the femur and tibia transected during knee arthroplasty were collected,and chondrocytes were isolated,cultured in vitro,and identified.(2)Cell counting kit-8 was used to detect the optimal intervention concentration of Complanatoside A in the concentration range of 0-160 μmol/L.(3)Chondrocytes were divided into blank group,sodium nitroprusside(1.5 mmol/L)-induced group,and sodium nitroprusside(1.5 mmol/L)+Complanatoside A(5 μmol/L)group.The viability and apoptosis rate of the cells in each group were detected by cell counting kit-8 and flow cytometry.The expression of type Ⅱ collagen and SOX9 was detected by immunofluorescence staining.The expression of apoptosis-related proteins and Wnt/β-catenin pathway proteins was detected by western blot assay. RESULTS AND CONCLUSION:The cells extracted in vitro were cultured and stained,and were clearly identified as chondrocytes.Complanatoside A had no obvious cytotoxicity to chondrocytes in the concentration range of 0-80 μmol/L,and significantly improved the chondrocyte viability in the concentration range of 2.5-10 μmol/L,especially when the concentration was 5 μmol/L.The apoptotic rate of chondrocytes was higher in the sodium nitroprusside-induced group than the blank control group,while the apoptotic rate was lower in the sodium nitroprusside+Complanatoside A group than the sodium nitroprusside-induced group.The fluorescence intensity of type Ⅱ collagen and SOX9 in chondrocytes was weaker in the sodium nitroprusside-induced group than the blank control group,while the fluorescence intensity of type Ⅱ collagen and SOX9 in the sodium nitroprusside+Complanatoside A group was higher than that of the sodium nitroprusside-induced group.In the sodium nitroprusside-induced group,the protein expression of Bax,Caspase-3,matrix metalloproteinase 13,Wnt3a,Wnt5a and β-catenin was higher than that of the blank control group,while the protein expression of Bcl-2 was lower than that of the blank control group.In the sodium nitroprusside+Complanatoside A group,except for the protein expression of Bcl-2 which was higher than that of the sodium nitroprusside-induced group,the expression of the other aforementioned proteins was lower than that of the sodium nitroprusside-induced group.To conclude,Complanatoside A has a certain inhibitory effect on chondrocyte apoptosis,which could regulate apoptosis-related proteins and promote the expression of chondrocyte regulatory factors,and presumably might play a role through inhibiting the Wnt/β-catenin signaling pathway.

Background When live working line operators engage in upper limb operations, working for a long time with raising arms and the exposure to adverse ergonomic factors tend to increase muscle load, cause fatigue accumulation, and increase the risk of work-related musculoskeletal disorders (WMSDs). Objective To analyze work posture and associated muscle fatigue during executing breaking/connecting contact terminal, and identify adverse ergonomic factors of the work process. Methods This study recruited 10 volunteers to perform breaking/connecting contact terminal simulation. At a distance of 4.5, 3.5, and 2.5 m from the body to the wire, each performed the task 5 times. Visual 3D was used to analyze the kinematic data from motion capture. The surface electromyography (sEMG) signals of the deltoid, biceps, triceps, and brachioradialis were recorded during the simulation and analyzed for muscle fatigue using root mean square (RMS), median frequency (MF), and jointed EMG amplitude and spectrum analysis (JASA). After completion of each task, Borg scale was used to query the volunteers of their subjective fatigue. A 2-min rest was required between each distance. Results The kinematic data from motion capture showed that in the entire process of the task, the right upper limb was higher when lifting, with the right shoulder joint maintaining flexion and fluctuating periodically between abduction and adduction, external and internal rotation, the right elbow joint maintaining flexion and supination. The frequency of task cycle showed a significant effect on the Borg scale scores (P<0.001, partial \begin{document}$ {\eta }^{2} $\end{document}=0.464); the distance showed no significant effect on the Borg scale scores (P>0.05, partial \begin{document}$ {\eta }^{2} $\end{document}=0.002); their interaction effect was not significant (P>0.05, partial \begin{document}$ {\eta }^{2} $\end{document}=0.020). The results of the sEMG signals showed that at a distance of 4.5 m, the volunteers had the highest percentages of maximal voluntary electrical activation (MVE%) in the deltoid and right brachioradialis and the lowest MF values in the deltoid and left brachioradialis after completing 5 task cycles. The results of JASA showed that fatigue was observed in brachioradialis and deltoid after completing 5 task cycles at a distance of 4.5 m, the right deltoid and right brachioradialis at a distance of 3.5 m, in the brachioradialis, deltoid, and left bicep at a distance of 2.5 m. Conclusion The subjective fatigue of workers who engaged in breaking/connecting contact terminal elevates with more repetitive operations. Based on the sEMG and motion capture analysis, it can be found that improper distance between the workers and the target work area can increase the burden from poor posture and improper use of work equipment, and lead to muscle fatigue; the deltoid and brachioradialis are the key muscles of fatigue in this type of operation; changing the angle of the elbow joint and the shoulder joint during the process of the operation can affect the deltoid and brachioradialis exertion and loading.

Background Power grid is an important component of the national infrastructure. The occupational health issues among the workers in this industry are attracting great concern nationwide. Objective To investigate the prevalence of work-related musculoskeletal disorders (WMSDs) in neck and shoulder among the power distribution workers of power supply enterprises, and analyze the related influencing factors. Method In April 2023, a total of 1244 workers in 50 municipal power supply bureaus were randomly selected from the three provinces under China Southern Power Grid using cluster sampling method. The questionnaire used in the study was based on a revised Musculoskeletal Disorders Questionnaire and added ergonomic load of upper limb work. \begin{document}$ {\chi }^{2} $\end{document} test and logistic regression model were used to explore the influencing factors of neck pain and shoulder pain among the subjects. Results A total of 1244 valid questionnaires were recovered and the effective recovery rate was 90.87%(1244/1369). The positive rates of neck pain and shoulder pain were 45.5% (566 cases) and 36.3% (452 cases) respectively. The logistic regression analysis results showed that more than 20 years working age (OR=2.27, 95%CI: 1.39, 3.96; OR=2.56, 95%CI: 1.53, 4.26), often (OR=2.08, 95%CI: 1.35, 3.20; OR=2.40, 95%CI: 1.50, 3.58)/quite often (OR=2.96, 95%CI: 1.73, 5.04; OR=2.72, 95%CI: 1.49, 4.94) maintaining a forced posture, and working immediately after break (OR=1.72, 95%CI: 1.04, 2.85; OR=2.14, 95%CI: 1.19, 3.88) were associated with a higher positive rate of neck pain and shoulder pain respectively. Feeling sufficient rest (OR=0.61, 95%CI: 0.47, 0.80; OR=0.63, 95%CI: 0.50, 0.83) and opportunity to decide when to take breaks (OR=0.72, 95%CI: 0.53, 0.98; OR=0.62, 95%CI: 0.41, 0.93) were associated with a lower positive rate of neck pain and shoulder pain respectively. Conclusion The positive rates of neck pain and shoulder pain are high among power distribution workers. The main influencing factors included long working age, quite often maintaining a forced posture, and working immediately after break.

OBJECTIVE To explore the effect and mechanism of Zhiqiao gancao decoction （ZQGCD） on pathological angiogenesis of degenerative intervertebral disc. METHODS The rats were randomly divided into sham operation group （normal saline）， model group （normal saline）， hypoxia inducible factor-1α （HIF-1α） inhibitor （YC-1） group [2 mg/（kg·d）， tail vein injection]， and ZQGCD low-dose， medium-dose and high-dose groups [3.06， 6.12， 12.24 g/（kg·d）]， with 8 rats in each group. Except for sham operation group， lumbar disc degeneration model of rat was constructed in all other groups. After modeling， they were given relevant medicine once a day， for consecutive 3 weeks. After the last medication， pathological changes and angiogenesis of the intervertebral disc tissue in rats were observed； the levels of inflammatory factors [interleukin-1β （IL-1β）， IL-6， tumor necrosis factor-α （TNF-α）] and the expressions of angiogenesis-related proteins [HIF-1α， vascular endothelial growth factor （VEGF）， VEGF receptor 2 （VEGFR2）， angiotensin 1（Ang 1）， Ang 2] in the com intervertebral disc tissue in rats were all determined. In cell experiment， the primary nucleus pulposus cells were isolated and cultured from rats， and cellular degeneration was induced using 50 ng/mL TNF-α. The cells were divided into blank control group （10% blank control serum）， TNF-α group （10% blank control serum）， YC-1 group （10% blank control serum+0.2 mmol/L YC-1）， and 5%， 10%， 15% drug-containing serum group （5%， 10%， 15% drug-containing serum）. After 24 hours of intervention， the nucleus pulposus cells were co-cultured with HUVEC. The expressions of Collagen Ⅱ， matrix metalloproteinase-3 （MMP-3） in nucleus pulposus cells were detected. HUVEC proliferation， migration and tube forming ability were detected， and the expression levels of the HIF-1α/VEGF/Ang signal axis and angiogenesis- related proteins （add MMP-2， MMP-9） in HUVEC were detected. RESULTS Animal experiments had shown that compared with model group， the positive expression of CD31 in the intervertebral disc tissues of rats in each drug group was down-regulated （P＜ 0.05）， the levels of inflammatory factors and angiogenesis-related proteins were decreased significantly （P＜0.05）， and the pathological changes in the intervertebral disc were alleviated. Cell experiments had shown that compared with TNF-α group， the expression of Collagen Ⅱ in nucleus pulposus cells of all drug groups was significantly up-regulated （P＜0.05）， and the expression of MMP-3 was significantly down-regulated （P＜0.05）； the proliferation， migration and tubulogenesis of HUVEC were significantly weakened （P＜0.05）. The mRNA and protein expressions of HIF-1α， VEGF， Ang 2 as well as the expression of angiogenesis-related proteins （except for the expression of Ang 2 mRNA and HIF-1α， VEGFR2， Ang 2 protein in 5% drug- containing serum group） were significantly down-regulated （P＜0.05）. CONCLUSIONS ZQGCD may inhibit the HIF-1α/VEGF/ Ang signal axis to weaken the angiogenic ability of vascular endothelial cells， improve pathological angiogenesis in the intervertebral disc， and delay the degeneration of the intervertebral disc.

This paper summarized professor WU Mianhua's experience in the treatment of tumors using Hehuanhua （Flos Albiziae）. He believes that the occurrence and development of tumors are closely related to emotions， and thereafter proposed the concept of "masses usually due to constraint， and should be treated by regulating the spirit".Hehuanhua is a light and aromatic flower that enters the heart， liver and spleen meridians， and is good at relieving constraint and regulating the spirit， harmonizing the center with aroma， which can be used to treat all kinds of tumor-related complications. Hehuanmi is flower buds， picked before the flowers fully blooms， have the effect of clearing and lightening upward， opening up the heart and mind， and unblocking liver qi. Commonly used formulas include self-made Ningxin Anmian Decoction （宁心安眠汤） to treat tumor-related insomnia， self-made Aitongxiao Formula （癌痛消方） to treat tumor-related pain， self-made Erhua Jieyu Formula （二花解郁方） to treat tumor-associated depression， and self-made Shugan Tiaohe Decoction （疏肝调和汤） to deal with peri-menopausal state after the treatment of tumors. Hehuanhua is an inflorescence， which captures the aromatic essence and has the function of removing the filth and turbidity， and can wake up the spleen and harmonize the stomach； therefore， it is often used in self-made Tiaomu Hezhong Decoction （调木和中汤） to treat chemotherapy-related digestive tract adverse reactions or combined with rose flowers to treat chemotherapy-induced oral ulcers.

Objective To investigate the global burden of visceral leishmaniasis (VL) from 1990 to 2021 and predict the trends in the burden of VL from 2022 to 2035, so as to provide insights into global VL prevention and control. Methods The global age-standardized incidence, prevalence, mortality and disability-adjusted life years (DALYs) rates of VL and their 95% uncertainty intervals (UI) were captured from the Global Burden of Disease Study 2021 (GBD 2021) data resources. The trends in the global burden of VL were evaluated with average annual percent change (AAPC) and 95% confidence interval (CI) from 1990 to 2021, and gender-, age-, country-, geographical area- and socio-demographic index (SDI)-stratified burdens of VL were analyzed. The trends in the global burden of VL were projected with a Bayesian age-period-cohort (BAPC) model from 2022 to 2035, and the associations of age-standardized incidence, prevalence, mortality, and DALYs rates of VL with SDI levels were examined with a smoothing spline model. Results The global age-standardized incidence [AAPC = -0.25%, 95% CI: (-0.25%, -0.24%)], prevalence [AAPC = -0.06%, 95% CI: (-0.06%, -0.06%)], mortality [AAPC = -0.25%, 95% CI: (-0.25%, -0.24%)] and DALYs rates of VL [AAPC = -2.38%, 95% CI: (-2.44%, -2.33%)] all appeared a tendency towards a decline from 1990 to 2021, and the highest age-standardized incidence [2.55/10⁵, 95% UI: (1.49/10⁵, 4.07/10⁵)], prevalence [0.64/10⁵, 95% UI: (0.37/10⁵, 1.02/10⁵)], mortality [0.51/10⁵, 95% UI: (0, 1.80/10⁵)] and DALYs rates of VL [33.81/10⁵, 95% UI: (0.06/10⁵, 124.09/10⁵)] were seen in tropical Latin America in 2021. The global age-standardized incidence and prevalence of VL were both higher among men [0.57/10⁵, 95% UI: (0.45/10⁵, 0.72/10⁵); 0.14/10⁵, 95% UI: (0.11/10⁵, 0.18/10⁵)] than among women [0.27/10⁵, 95% UI: (0.21/10⁵, 0.33/10⁵); 0.06/10⁵, 95% UI: (0.05/10⁵, 0.08/10⁵)], and the highest mortality of VL was found among children under 5 years of age [0.24/10⁵, 95% UI: (0.08/10⁵, 0.66/10⁵)]. The age-standardized incidence (r = -0.483, P < 0.001), prevalence (r = -0.483, P < 0.001), mortality (r = -0.511, P < 0.001) and DALYs rates of VL (r = -0.514, P < 0.001) correlated negatively with SDI levels from 1990 to 2021. In addition, the global burden of VL was projected with the BAPC model to appear a tendency towards a decline from 2022 to 2035, and the age-standardized incidence, prevalence, mortality and DALYs rates were projected to be reduced to 0.11/10⁵, 0.03/10⁵, 0.02/10⁵ and 1.44/10⁵ in 2035, respectively. Conclusions Although the global burden of VL appeared an overall tendency towards a decline from 1990 to 2021, the burden of VL showed a tendency towards a rise in Central Asia and western sub-Saharan African areas. The age-standardized incidence and prevalence rates of VL were relatively higher among men, and the age-standardized mortality of VL was relatively higher among children under 5 years of age. The global burden of VL was projected to continue to decline from 2022 to 2035.

Epilepsy is a chronic neurological disease caused by abnormal synchronous discharge of the brain, which is characterized by recurrent and transient neurological abnormalities, mainly manifested as loss of consciousness and limb convulsions, and can occur in people of all ages. At present, anti-epileptic drugs (AEDs) are still the main means of treatment, but their efficacy is limited by the problem of drug resistance, and long-term use can cause serious side effects, such as cognitive dysfunction and vital organ damage. Although surgical resection of epileptic lesions has achieved certain results in some patients, the high cost and potential risk of neurological damage limit its scope of application. Therefore, the development of safe, accurate and personalized non-invasive treatment strategies has become one of the key directions of epilepsy research. In recent years, photobiomodulation (PBM) has gained significant attention as a promising non-invasive therapeutic approach. PBM uses light of specific wavelengths to penetrate tissues and interact with photosensitive molecules within cells, thereby modulating cellular metabolic processes. Research has shown that PBM can enhance mitochondrial function, promote ATP production, improve meningeal lymphatic drainage, reduce neuroinflammation, and stimulate the growth of neurons and synapses. These biological effects suggest that PBM not only holds the potential to reduce the frequency of seizures but also to improve the metabolic state and network function of neurons, providing a novel therapeutic avenue for epilepsy treatment. Compared to traditional treatment methods, PBM is non-invasive and avoids the risks associated with surgical interventions. Its low risk of significant side effects makes it particularly suitable for patients with drug-resistant epilepsy, offering new therapeutic options for those who have not responded to conventional treatments. Furthermore, PBM’s multi-target mechanism enables it to address a variety of complex etiologies of epilepsy, demonstrating its potential in precision medicine. In contrast to therapies targeting a single pathological mechanism, PBM’s multifaceted approach makes it highly adaptable to different types of epilepsy, positioning it as a promising supplementary or alternative treatment. Although animal studies and preliminary clinical trials have shown positive outcomes with PBM, its clinical application remains in the exploratory phase. Future research should aim to elucidate the precise mechanisms of PBM, optimize light parameters, such as wavelength, dose, and frequency, and investigate potential synergistic effects with other therapeutic modalities. These efforts will be crucial for enhancing the therapeutic efficacy of PBM and ensuring its safety and consistency in clinical settings. This review summarizes the types of epilepsy, diagnostic biomarkers, the advantages of PBM, and its mechanisms and potential applications in epilepsy treatment. The unique value of PBM lies not only in its multi-target therapeutic effects but also in its adaptability to the diverse etiologies of epilepsy. The combination of PBM with traditional treatments, such as pharmacotherapy and neuroregulatory techniques, holds promise for developing a more comprehensive and multidimensional treatment strategy, ultimately alleviating the treatment burden on patients. PBM has also shown beneficial effects on neural network plasticity in various neurodegenerative diseases. The dynamic remodeling of neural networks plays a critical role in the pathogenesis and treatment of epilepsy, and PBM’s multi-target mechanism may promote brain function recovery by facilitating neural network remodeling. In this context, optimizing optical parameters remains a key area of research. By adjusting parameters such as wavelength, dose, and frequency, researchers aim to further enhance the therapeutic effects of PBM while maintaining its safety and stability. Looking forward, interdisciplinary collaboration, particularly in the fields of neuroscience, optical engineering, and clinical medicine, will drive the development of PBM technology and facilitate its transition from laboratory research to clinical application. With the advancement of portable devices, PBM is expected to provide safer and more effective treatments for epilepsy patients and make a significant contribution to personalized medicine, positioning it as a critical component of precision therapeutic strategies.

Background Unhealthy lifestyle behaviors may be associated with an increased risk of cardiometabolic risk factor aggregation (CMRF≥ 2), and few studies have focused on the correlation between the two in occupational populations. Objective To investigate the current status of CMRF≥2 and the compliance of healthy lifestyle in male occupational personnel, explore the effect of lifestyle on cardiometabolic risk, and provide reference for formulating healthy behavior promotion strategies and reducing cardiometabolic risk in occupational populations. Methods The study subjects were selected from male workers who completed occupational health examinations at an occupational disease prevention and control hospital in Shanxi Province from May to December 2023, and 15125 study subjects aged 18−60 years were finally included according to pre-determined inclusion and exclusion criteria. All subjects received a series of assessments including questionnaires (basic information, lifestyle habits, and occupational factors), physical examination, laboratory tests, and six cardiometabolic risk factors (central obesity, hypertension, type 2 diabetes, hypertriglyceridemia, low-density lipoprotein cholesterolemia, and hyperuricemia). A healthy lifestyle score was calculated based on six behavioral factors (smoking, drinking, physical activity, diet, sleep, sedentary behavior) and 1 point for one positive healthy behavior. The enrolled workers were then divided into three groups according to their total scores: 0−1 points (poor group), 2−3 points (moderate group), and 4−6 points (good group). Logistic regression models were used to analyze the statistical associations between lifestyle and CMRF≥2. Results The median age of the 15125 male study participants was 40 years, and the positive rate of CMRF≥2 was 53.5%. Adherence to moderate alcohol consumption was the most compliant healthy behavior (79.4%), followed by current non-smoking (41.7%), while adherence to adequate sedentary behavior (23.6%) and healthy eating (21.1%) were relatively low, and only 17.4% were able to adhere to four or more healthy lifestyle behaviors. After adjusting for confounders, when compared with the poor group high lifestyle score was found to be a protective factor for CMRF≥2 (moderate group: OR=0.70, 95%CI: 0.63, 0.77; good group: OR=0.66, 95%CI: 0.58, 0.75). In stratified analyses across different job types (coal miners, auxiliary workers, ground workers, and others), occupational stress (with or without), shift patterns (day shift, night shift, or rotating shift), dust exposure (with or without), and noise exposure (with or without), individuals with higher lifestyle scores exhibited a consistently lower risk of CMRF≥2. There was an interaction between shift pattern and lifestyle on CMRF≥2 (P_interaction<0.05). Conclusion This occupational group has a high positive rate of CMRF≥2 and a high prevalence of poor lifestyles with low adherence to some healthy behaviors. High healthy lifestyle scores are associated with a lower risk of aggregation of cardiometabolic risk factors, which may be reduced through lifestyle interventions.

Objective To investigate the effect of sodium-glucose cotransporter 2 inhibitor (empagliflozin, EMPA) on myocardial remodeling in a mouse uremic cardiomyopathy (UCM) model induced by 5/6 nephrectomy, through the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (PKB/AKT)/p65 signaling pathway. Methods The animals were divided into three groups: Sham group (n=6), UCM group (n=8), and UCM＋EMPA group (n=8). A UCM model was established in C57BL/6N mice using the 5/6 nephrectomy. Starting from 5 weeks post-surgery, EMPA or a placebo was administered. After 16 weeks, blood pressure, serum creatinine, blood urea nitrogen, 24-hour urine glucose and urine sodium were measured. Cardiac structure and function were assessed by echocardiography. Hematoxylin-eosin (HE) staining and Masson trichrome staining were used to observe pathological changes in the heart and kidneys. Wheat germ agglutinin (WGA) staining was used to evaluate myocardial hypertrophy. The real-time quantitative PCR (RT-qPCR) was used to detect the expression levels of myocardial hypertrophy- and fibrosis-related mRNAs. Western blotting was used to detect the expression levels of PI3K, AKT and p65 in myocardial tissues. Results After 16 weeks, UCM group exhibited significantly higher blood pressure, serum creatinine, blood urea nitrogen than sham group (P＜0.01); UCM＋EMPA group exhibited lower blood pressure, serum creatinine, blood urea nitrogen, and higher 24 h urine sodium and glucose than UCM group (P＜0.05). Echocardiographic results showed ventricular remodeling in the UCM group, evidenced by left ventricular wall thickening, left ventricular enlargement, increased left ventricular mass, and decreased systolic function (P＜0.05); ventricular remodeling was alleviated (P＜0.05), though there was no significant improvement in systolic function in UCM＋EMPA group. HE and Masson stainings revealed myocardial degeneration, necrosis, and interstitial fibrosis in UCM group (P＜0.01); the myocardial pathology improved with reduced collagen deposition in UCM＋EMPA group (P＜0.01). WGA staining confirmed myocardial hypertrophy in UCM group (P＜0.01), while myocardial hypertrophy was alleviated in UCM＋EMPA group (P＜0.01). RT-qPCR results showed myocardial hypertrophy- and fibrosis-related genes (NPPA, NPPB, MYH7, COL1A1, COL3A1, TGF-β1) were upregulated in UCM group (P＜0.05), but downregulated in UCM＋EMPA group. Western blotting showed PI3K, p-AKT/AKT ratio, and p-p65/p65 ratio were increased in UCM group, but decreased in UCM＋EMPA group (P＜0.05). Conclusion EMPA can improve myocardial hypertrophy and fibrosis in the UCM mouse model, and it may play the role through inhibiting the PI3K/AKT/p65 signaling pathway.