ObjectiveTo investigate the effects of the classical Chinese medicine compound prescription Erjingwan on the inflammatory response and apoptosis of skeletal muscle cells in a mouse model of sarcopenia and decipher the mechanism based on the silent information regulator 1 （SIRT1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway. MethodsForty C57/BL6 male mice were randomized into a control group， a model group， and groups with different doses of Erjingwan （8，16，32 g·kg^-1）. The mouse model of sarcopenia was established by D-gal-induced skeletal muscle senescence. The body weight and grip strength of mice treated with different doses of Erjingwan were examined to evaluate their physiological functions. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathological changes and fibrosis in the skeletal muscle of mice. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum samples of mice， and biochemical tests were conducted to quantify the levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， and glutathione （GSH） in the serum. The protein and mRNA levels of SIRT1， Nrf2， B-cell lymphoma （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsAfter 4 weeks of drug intervention， the model group exhibited significant reductions in body weight and grip strength （P0.01） compared with the control group. Compared with the model group， all doses of Erjingwan increased the body weight in mice at week 8 （P0.01） and grip strength from week 6 （P0.01）. HE staining revealed clear muscle fiber structure in the control group， muscle fiber rupture and atrophy in the model group， and dose-dependent repair of muscle fiber structure in the Erjingwan groups. Masson staining showed minimal collagen fibers and mild fibrosis in the control group， collagen fiber proliferation and severe fibrosis in the model group， and collagen proliferation with dose-dependent inhibition of fibrosis in the Erjingwan groups. ELISA results showed that serum levels of TNF-α and IL-6 were elevated in the model group compared with those in the control group （P0.01）. After intervention， the low-dose Erjingwan group exhibited a decreased TNF-α level （P0.05）， while the medium and high-dose groups showed decreases in both TNF-α and IL-6 levels （P0.01）. Biochemical assays revealed that the model group had decreased SOD and GSH levels （P0.01） and an increased MDA level （P0.01） compared with the control group. The medium and high-dose Erjingwan groups exhibited increases in SOD and GSH levels （P0.01） and decreases in MDA level （P0.01）， compared with the model group. WB and Real-time PCR results showed that compared with the control group， the model group presented down-regulated protein and mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 in the muscle tissue （P0.01） and up-regulated protein and mRNA levels of Bax （P0.01）. Compared with the model group， Erjingwan at different doses up-regulated the protein levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01） and down-regulated the protein and mRNA levels of Bax （P0.01） in the muscle tissue. Low-dose Erjingwan elevated the mRNA levels of Nrf2 and HO-1 （P0.05， P0.01）， and medium and high-dose Erjingwan up-regulated the mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01）. ConclusionErjingwan reduced the content of inflammatory factors in skeletal muscle cells， improved the antioxidant capacity， and attenuated pathological changes and fibrosis in the muscle of the mouse model of sarcopenia by regulating the SIRT1/Nrf2/HO-1 pathway， inflammatory response， and apoptosis network.

ObjectiveTo investigate the effects of the classical Chinese medicine compound prescription Erjingwan on the inflammatory response and apoptosis of skeletal muscle cells in a mouse model of sarcopenia and decipher the mechanism based on the silent information regulator 1 （SIRT1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway. MethodsForty C57/BL6 male mice were randomized into a control group， a model group， and groups with different doses of Erjingwan （8，16，32 g·kg^-1）. The mouse model of sarcopenia was established by D-gal-induced skeletal muscle senescence. The body weight and grip strength of mice treated with different doses of Erjingwan were examined to evaluate their physiological functions. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathological changes and fibrosis in the skeletal muscle of mice. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum samples of mice， and biochemical tests were conducted to quantify the levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， and glutathione （GSH） in the serum. The protein and mRNA levels of SIRT1， Nrf2， B-cell lymphoma （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsAfter 4 weeks of drug intervention， the model group exhibited significant reductions in body weight and grip strength （P0.01） compared with the control group. Compared with the model group， all doses of Erjingwan increased the body weight in mice at week 8 （P0.01） and grip strength from week 6 （P0.01）. HE staining revealed clear muscle fiber structure in the control group， muscle fiber rupture and atrophy in the model group， and dose-dependent repair of muscle fiber structure in the Erjingwan groups. Masson staining showed minimal collagen fibers and mild fibrosis in the control group， collagen fiber proliferation and severe fibrosis in the model group， and collagen proliferation with dose-dependent inhibition of fibrosis in the Erjingwan groups. ELISA results showed that serum levels of TNF-α and IL-6 were elevated in the model group compared with those in the control group （P0.01）. After intervention， the low-dose Erjingwan group exhibited a decreased TNF-α level （P0.05）， while the medium and high-dose groups showed decreases in both TNF-α and IL-6 levels （P0.01）. Biochemical assays revealed that the model group had decreased SOD and GSH levels （P0.01） and an increased MDA level （P0.01） compared with the control group. The medium and high-dose Erjingwan groups exhibited increases in SOD and GSH levels （P0.01） and decreases in MDA level （P0.01）， compared with the model group. WB and Real-time PCR results showed that compared with the control group， the model group presented down-regulated protein and mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 in the muscle tissue （P0.01） and up-regulated protein and mRNA levels of Bax （P0.01）. Compared with the model group， Erjingwan at different doses up-regulated the protein levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01） and down-regulated the protein and mRNA levels of Bax （P0.01） in the muscle tissue. Low-dose Erjingwan elevated the mRNA levels of Nrf2 and HO-1 （P0.05， P0.01）， and medium and high-dose Erjingwan up-regulated the mRNA levels of SIRT1， Nrf2， HO-1， and Bcl-2 （P0.01）. ConclusionErjingwan reduced the content of inflammatory factors in skeletal muscle cells， improved the antioxidant capacity， and attenuated pathological changes and fibrosis in the muscle of the mouse model of sarcopenia by regulating the SIRT1/Nrf2/HO-1 pathway， inflammatory response， and apoptosis network.

ObjectiveTo predict the mechanism through which Shasheng Maidong Tang enhances the efficacy of chemotherapy for lung cancer via network pharmacology and validate the prediction results in animal experiments. MethodsThe potential mechanism through which Shasheng Maidong Tang enhances the efficacy of chemotherapy for lung cancer was predicted by network pharmacology， liquid chromatography-mass spectrometry （LC-MS）， and molecular docking methods. C57/BL6 mice were assigned into normal， model， cisplatin， and Shasheng Maidong Tang+cisplatin groups. In addition to the normal group， the remaining groups were injected subcutaneously with 0.2 mL of 1×10⁷ cells·mL^-1 Lewis lung cancer cells to establish the Lewis lung cancer model. The daily gavage dose of Shasheng Maidong Tang was 3.58 g·kg^-1， and the concentration of cisplatin intraperitoneally injected on every other day was 2 mg·kg^-1. Drugs were administered for 14 d. The changes in the tumor volume and the rate of tumor suppression were monitored， and the tumor histopathological changes were observed by hematoxylin-eosin （HE） staining. Enzyme-linked immunosorbent assay was employed to measure the interleukin （IL）-6 and interferon （IFN）-γ levels in peripheral blood. Real-time PCR was performed to quantify the mRNA levels of Janus kinase 2 （JAK2）， signal transducer and activator of transcription 1 （STAT1）， and signal transducer and activator of transcription 3 （STAT3） in the tumor tissue of mice. Western blot was employed to determine the protein levels of JAK2， STAT3， B-cell lymphoma-2 （Bcl-2）， cysteinyl aspartate-specific proteinase-3 （Caspase-3）， and Pim-1 proto1 （PIM1） in the tumor tissue. Immunohistochemistry was employed to detect the expression of Bcl-2 and PIM1 in the tumor tissue. ResultsNetwork pharmacological predictions indicated that Shasheng Maidong Tang might enhance the efficacy of chemotherapy for lung cancer by regulating nitrogen metabolism， AGE-RAGE signaling pathway， cancer pathway， and JAK/STAT signaling pathway. The experimental results demonstrated that tumor volume in the cisplatin group and Shasheng Maidong Tang+cisplatin group was reduced compared with the model group， with statistically distinct differences observed on days 14， 17， 20 post modeling （P<0.05）. Notably， the Shasheng Maidong Tang+cisplatin therapy further decreased tumor volume compared with the cisplatin group， showing marked reductions on days 17 and 20 （P<0.05）， consistent with trends visualized in tumor volume comparison charts. The Shasheng Maidong Tang+cisplatin group exhibited higher tumor inhibition rate than the cisplatin group （P<0.05）. Histopathological analysis via HE staining revealed that the tumors in the model group displayed frequent nuclear mitosis， densely arranged cells， hyperchromatic nuclei， and no necrosis. Cisplatin treatment induced partial necrosis and vacuolization， while the Shasheng Maidong Tang+cisplatin group exhibited extensive necrotic regions， maximal vacuolization， disarranged tumor cells， and minimal mitotic activity. Compared with the model group， the cisplatin group and the Shasheng Maidong Tang+cisplatin group showed elevated level of IFN-γ （P<0.01） and declined level of IL-6 （P<0.01） in the peripheral blood. Compared with the cisplatin group， the Shasheng Maidong Tang+cisplatin group presented elevated level of IFN-γ （P<0.01） and lowered level of IL-6 （P<0.01） in the peripheral blood. Compared with the model group， the cisplatin group and the Shasheng Maidong Tang+cisplatin groups showed down-regulated mRNA levels of JAK2 and STAT3 （P<0.01） and up-regulated mRNA level STAT1 （P<0.01）. Compared with the cisplatin group， the Shasheng Maidong Tang+cisplatin group presented down-regulated mRNA levels of JAK2 and STAT3 （P<0.01） and up-regulated mRNA level of STAT1 （P<0.01）. Compared with the model group， the cisplatin group and the Shasheng Maidong Tang+cisplatin group showed down-regulated protein levels of JAK2 （P<0.01）， Bcl-2 （P<0.01）， PIM1 （P<0.01）， and STAT3 （P<0.05）， and up-regulated protein level of Caspase-3 （P<0.01）. Compared with the cisplatin group， Shasheng Maidong Tang+cisplatin group presented down-regulated protein levels of JAK2 （P<0.01）， Bcl-2 （P<0.01）， PIM1 （P<0.01）， STAT3 （P<0.05）， and up-regulated protein level of Caspase-3 （P<0.01）. The Bcl-2 and PIM1 expression results obtained by immunohistochemistry were consistent with those of Western blot. ConclusionShasheng Maidong Tang may enhance the efficacy of chemotherapy in the mouse model of Lewis lung cancer by regulating the JAK2/STAT3 signaling pathway.

Objective To investigate the effect and mechanism of the signal transducer and activator of transcription 3 (STAT3) inhibitor Stattic on the rejection of mouse heart allograft. Methods BALB/c mice (donors) were used to transplant skin onto C57BL/6 mice (recipients). Four weeks later, memory CD4⁺ T cells (CD4⁺Tm) were isolated from the recipient mice's spleens. Mixed lymphocyte reaction experiment was conducted with C57BL/6 mouse splenocytes and CD4⁺Tm, and the EdU method was used to detect the effect of Stattic on CD4⁺Tm cell proliferation. A C57BL/6 mouse heart transplant (HTx) model was constructed, and the experiment was divided into four groups: Non-HTx group, HTx group, Tm/HTx group, and Tm/HTx+Stattic group. The survival of heart allografts in mice was observed daily. Hematoxylin-eosin staining was used to observe the histopathology of the heart allografts. Real-time fluorescent quantitative polymerase chain reaction was used to detect the expression levels of interferon (IFN)-γ, interleukin (IL)-2, IL-10, and transforming growth factor-β1 (TGF-β1) messenger RNA (mRNA) in the heart allografts. Enzyme-linked immunosorbent assay was used to detect the levels of IFN-γ, IL-2, IL-10, and TGF-β1 in the serum. Flow cytometry was used to detect the levels of CD4⁺Tm (CD4⁺CD44⁺CD62L⁺) in splenic lymphocytes. And Western blotting was used to detect the expression levels of STAT3 and p-STAT3 proteins in the heart allografts. Results When the concentration of Stattic exceeded 2.5 μmol/L, it could inhibit the proliferation of CD4⁺Tm cells. Compared with the HTx group, the Tm/HTx group showed shorter survival time of heart grafts, more severe histopathological damage, increased serum IFN-γ and IL-2 levels, decreased IL-10 and TGF-β1 levels, increased relative expression of IFN-γ and IL-2 mRNA, decreased relative expression of IL-10 and TGF-β1 mRNA in the heart allografts, increased proportion of CD4⁺Tm in splenic lymphocytes, and increased p-STAT3/STAT3 ratio in the heart allografts (all P<0.05). Compared with the Tm/HTx group, the Tm/HTx+Stattic group showed longer survival time of heart grafts, less severe histopathological damage, decreased serum IFN-γ and IL-2 levels, increased IL-10 and TGF-β1 levels, decreased relative expression of IFN-γ and IL-2 mRNA, increased relative expression of IL-10 and TGF-β1 mRNA in the heart allografts, decreased proportion of CD4⁺Tm in splenic lymphocytes, and decreased p-STAT3/STAT3 ratio in the heart allografts (all P<0.05). Conclusions Stattic may prolong the survival time of mouse heart allografts, and its mechanism may be related to the inhibition of CD4⁺Tm- mediated acute rejection.

Objective: To explore the relationship of family function with sleep and externalizing problem behaviors of preschool children, so as to provide a guidance for externalizing problem prevention and intervention among preschool children. Methods: From October 2023 to January 2024, a convenience sampling method was used to select 5 138 preschool children from kindergartens in 8 districts of Wuhan City, Hubei Province. Parents completed the survey for Family Adaptability and Cohesion Scale, children s sleep habits and Child Behavior Checklist (CBCL). Spearman correlation analysis was used to examine the correlation of family function with scores of sleep quality and externalizing problem behaviors among preschool children. A mediation model analysis and bootstrap test were conducted to further investigate the mediating role of sleep quality between family function and externalizing problem behaviors. Mplus 8.7 software was used for latent profile analysis of family function. Results: The reported rates of poor sleep quality and externalizing problem behaviors among preschool children were 11.8% ( n =607), 20.0% ( n =1 026). The relevant analysis results showed that family function was negatively correlated with sleep quality and externalizing problem behaviors ( r = -0.20, -0.23), and sleep quality was positively correlated with externalizing problem behaviors ( r =0.27) ( P <0.01). The mediation effect test showed that family function negatively predicted externalizing problem behaviors ( β =-0.079) and sleep quality ( β = -0.075), while sleep quality positively predicted externalizing problem behaviors ( β =0.215) ( P <0.01). The latent profile analysis results showed that family function could be classified into 4 categories: high family function group (23.01%), upper middle family function group (44.65%), moderate family function group (26.24%) and low family function group (6.11%). Compared to high family function, the other three categories significantly positively predicted externalizing problem behaviors, and the mediating effects of sleep quality on different categories of family function were statistically significant [upper middle family function: mediation effect value was 0.022 (95% CI =0.004-0.041) and direct effect value was 0.329 (95% CI =0.263-0.396); middle family function: mediation effect value was 0.087 (95% CI =0.063-0.115) and direct effect value was 0.491 (95% CI =0.416-0.565); low family function: mediation effect value was 0.144 (95% CI =0.107-0.185) and direct effect 0.621 (95% CI =0.503-0.740)] ( P < 0.05 ). Conclusion Family function negatively predicts the externalizing problem behaviors of preschool children, and sleep quality plays a partial mediating role.

ObjectiveUltra performance liquid chromatography-quadrupole-time of flight tandem mass spectrometry （UPLC-Q-TOF-MS/MS） coupled with network pharmacology and molecular docking was utilized to explore the efficacy and mechanism of action of Ermiao Situ decoction on rats with damp-heat eczema. MethodsA rat model of damp-heat eczema was established by artificial climate chamber intervention combined with sensitization induction by dinitrochlorobenzene （DNCB）， and it was randomly divided into the normal group， the model group， the medium- and high-dose groups of Ermiao Situ decoction （3.40 g·kg^-1 and 6.80 g·kg^-1）， and the prednisone acetate group （2.51 mg·kg^-1）， with eight rats in each group， totalling 46 rats， of which six rats were tested with the drug-containing serum. The chemical analysis of drug-containing serum from rats was carried out by UPLC-Q-TOF-MS/MS， combined with network pharmacology for the prediction of key components， core targets， and signaling pathways， and molecular docking experiments were performed by CB-Dock2 online website. The pharmacological effects of Ermiao Situ decoction in the treatment of damp-heat eczema were investigated by epitaxial indexes combined with the pathologic tissue staining method. The serum levels of gastrin （GAS）， interleukin-4 （IL-4）， and interleukin-13 （IL-13） were measured by enzyme-linked immunosorbent assay （ELISA）. Interleukin-6 （IL-6）， Janus kinase 1 （JAK1）， phosphorylated （p）-JAK1， signal transduction and activation of transcription factor 3 （STAT3）， and p-STAT3 protein expression level was determined by Western bolt. ResultsA total of 19 active ingredients were detected in drug-containing serum samples of rats， which were predicted to act on 198 targets for the treatment of damp-heat eczema， among which the key ingredients included rhodopsin， huangpai alkaloids， and quercetin， and the main core targets included STAT3， tumor necrosis factor （TNF）， and IL-6， which were mainly involved in the cancer signaling pathway， phosphatidylinositol 3-kinase （PI3K）/protein kinase （Akt） signaling pathway， T helper 17 （Th17） cell differentiation signaling pathway， and JAK/STAT signaling pathway. The molecular docking results suggested that the key components had strong binding activities with the core targets IL-6， JAK1， and STAT3 in the JAK/STAT signaling pathway. The results of animal experiments showed that compared with those in the normal group， rats in the model group were depressed. They had loose hair， loose stools， epidermal oozing， vesiculation， and generation of thick scabs in the form of scales， decreased body weight， increased anus temperature and water intake， and increased indexes of the spleen， thymus gland， and stomach （P<0.05， P<0.01）， and the lesion tissue could be seen to be hyperkeratotic， with the aggregation of inflammatory cells and nonsignificant separation of epidermis and dermis. The gastric mucosa was thinned， deficient， and structurally disorganized， and obvious inflammatory cell aggregation was seen. The levels of GAS， IL-4， and IL-13 in serum were significantly reduced （P<0.05， P<0.01）， and the protein expression levels of IL-6， JAK1， p-JAK1， and p-STAT3 in the lesion tissue were significantly increased （P<0.05， P<0.01）. Compared with those in the model group， rats in each administration group had stable mental states， formed feces， a clean perianal area， and basically normal epidermis. Only a small amount of scaly scabs existed， and the rats had body weight increased， with decreased anal temperature and water intake， as well as decreased spleen， thymus， and gastric indexes （P<0.05， P<0.01）. Epidermal thickness was decreased， and epidermal and dermal separation boundaries were obvious， but hyperkeratotic and accumulation of inflammatory cells could still be seen. The thickness of gastric mucosa increased， and the structure was restored to varying degrees. The levels of GAS， IL-4， and IL-13 content in the serum of rats were increased to varying degrees， and the protein expression levels of IL-6， JAK1， p-JAK1， and p-STAT3 in the dermal lesion tissue were significantly decreased （P<0.05， P<0.01）. ConclusionErmiao Situ decoction may exert therapeutic effects on rats with damp-heat eczema by modulating the JAK/STAT signaling pathway.

Objective To explore the correlation between serum ferritin and the risk of metabolic syndrome, and to provide evidence for the prevention and control of metabolic syndrome. Methods Data was from the Jiang'an District survey data of the Chinese Resident Nutrition and Health Monitoring Project in 2022. A total of 399 adult residents were selected as the study subjects and the investigation was performed by questionnaire, physical examination and biochemical testing. Statistical analysis was conducted by SAS 9.4 software, and the association between serum ferritin and metabolic syndrome was analyzed by using multivariate logistic regression. Results The prevalence of metabolic syndrome in the study population was 43.61%, and 39.04% after standrdization. With the increase of serum ferritin levels, the prevalence of metabolic syndrome gradually increased (P<0.05). Serum ferritin was positively correlated with WC, DBP, TG, FPG, hsCRP, and HbA1c, while negatively correlated with HDL-C (P<0.05). Multivariate logistic regression analysis showed that after adjusting for confounding factors, female serum ferritin was positively correlated with the prevalence of metabolic syndrome (OR=3.59，95% CI：1.72-7.46); however, male serum ferritin level was not correlated with the prevalence of metabolic syndrome (OR=2.02，95% CI：0.76-3.40). Conclusion The prevalence of metabolic syndrome among residents in Jiang'an District is relatively high. Serum ferritin is associated with various components of metabolic syndrome, and the high serum ferritin level in women is associated with a higher risk of metabolic syndrome.

Dignity is a core concept in bioethics. With the development of emerging life science technologies， maintaining human dignity has become the main reason for restricting the use and development of these new technologies. In bioethics， this dignity-based conservatism manifests in two forms， namely religious conservatism and secular conservatism. However， they face some difficulties respectively. Compared with conservatism， the concept of dignity advocated by the capability approach can not only avoid these difficulties but also provide a reasonable justification for people’s rational utilization and development of emerging biotechnologies.

OBJECTIVE To investigate the effect and mechanism of bumetanide on lung injury in chronic obstructive pulmonary disease （COPD） model rats. METHODS COPD rat model was induced by lipopolysaccharide， and they were randomly divided into model group （COPD group）， bumetanide low-dose and high-dose groups （Bumetanide-L group， Bumetanide-H group）， bumetanide high-dose+Yes-associated protein/transcriptional coactivator containing PDZ-binding motif （YAP/TAZ） signaling pathway activator group （Bumetanide-H+PY-60 group）， with 12 rats in each group. Another 12 normal rats were selected as normal control group （Control group）. Thirty minutes before modeling， bumetanide/normal saline was inhaled or/and PY-60/ normal saline was injected into the tail vein. On the next day after the completion of modeling and drug administration， the pulmonary function index of the rats in each group was measured [forced expiratory volume in 0.3 seconds （FEV0.3）， forced vital capacity （FVC）， peak expiratory flow （PEF）， FEV0.3/FVC]. The levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6） and IL-1β in bronchoalveolar lavage fluid （BALF） were determined； the pathological morphology of lung tissue and degree of pulmonary fibrosis were observed. The expression levels of transforming growth factor- β （TGF- β）， α -smooth muscle actin （α-SMA） and TAZ protein as well as the phosphorylation of YAP protein in lung tissues were detected. RESULTS Compared with COPD group， the pathological injury of lung tissue in Bumetanide-L and Bumetanide-H groups was alleviated； the exfoliation of lung epithelial cells， tube wall thickening and the degree of pulmonary fibrosis were alleviated； inflammatory cell infiltration was reduced， and blue collagen deposition was reduced； FEV0.3， FVC， FEV0.3/FVC and PEF were significantly increased， while the lung injury score， levels of TNF-α， IL-6， IL-1β， expression levels of TGF-β， α-SMA and TAZ protein and the phosphorylation of YAP protein were significantly decreased （P＜0.05）. PY-60 could significantly reverse the improvement effects of bumetanide on above indexes （P＜0.05）. CONCLUSIONS Bumetanide can alleviate lung injury， inflammatory response and pulmonary fibrosis in COPD rats， and its mechanism is related to inhibiting YAP/TAZ signaling pathway.

Background With the continuous development of the healthcare industry, healthcare workers face increasing pressure, including long-term shift work and workplace violence from patients or their relatives. This not only affects the physical and mental health of healthcare workers but may also negatively impact the quality of patient care and the efficiency of medical services. Objectives To analyze the pathways through which shift work and workplace violence affect healthcare workers' self-rated health and depression symptoms, explore potential mediating role of job burnout, and conduct subgroup analyses to reveal differences among various groups. Methods Data were collected from 3706 frontline healthcare workers across 23 provinces from January 10 to February 5, 2019, using a snowball sampling method. The survey included basic demographic information, self-rated health, depression symptoms [assessed using the Patient Health Questionnaire-2 (PHQ-2)], workplace violence experience assessed using the Workplace Violence Scale), and job burnout (assessed using the Chinese Maslach Burnout Inventory). Data were analyzed using logistic regression, structural equation modeling (for mediating effects), and subgroup analysis to examine the impacts of shift work and workplace violence on health and depression symptoms. Results Among the subjects, 2700 workers (73.29%) reported shift work experience, 2079 workers (56.43%) experienced workplace violence, 633 workers (17.18%) reported poor self-rated health, and 687 workers (18.65%) reported depression symptoms. Shift work was associated with self-rated health (OR=0.572, 95%CI: 0.461, 0.710) and depression symptoms (OR=1.519, 95%CI: 1.190, 1.938), while workplace violence also associated with self-rated health (OR=0.566, 95%CI: 0.471, 0.681) and depression symptoms (OR=2.096, 95%CI: 1.740, 2.525). Job burnout significantly mediated the effects of shift work and workplace violence on self-rated health (indirect effects: −0.023, −0.027) and depression symptoms (indirect effects: 0.032, 0.037) (all P < 0.001). The subgroup analysis revealed that age, marital status, physical exercise, smoking, and alcohol consumption influenced the impacts of shift work and workplace violence on health. Conclusion Shift work and workplace violence significantly affect healthcare workers' self-rated health and depression symptoms, with job burnout playing a key mediating role in this process. This suggests that healthcare institutions should improve resource allocation, provide flexible scheduling systems, ensure adequate rest time, and increase psychological support and safety measures to help healthcare workers better cope with work-related stress and violence.