ObjectiveTo explore the role of cucurbitacin B （CuB） in inducing ferroptosis in 4T1 cells and its mechanism. MethodsThe effects of CuB（0.2， 0.4， 0.8 μmol·L^-1）on the proliferation ability of 4T1 cells in vitro were detected using the methyl thiazolyl tetrazolium （MTT） assay. The clonogenic ability of 4T1 cells was detected by the plate cloning assay， and the levels of lactate dehydrogenase （LDH） in 4T1 cells were detected by the use of a kit. The mitochondrial membrane potential and reactive oxygen species （ROS） levels in 4T1 cells were detected by flow cytometry， and the mitochondrial ultrastructure of 4T1 cells was observed by transmission electron microscopy. The western blot was used to detect the expression of ferroptosis-related protein p53 in 4T1 cells， solute carrier family 7 member 11 （SCL7A11）， glutathione peroxidase 4 （GPX4）， long-chain acyl-CoA synthetase 4 （ACSL4）， transferrin receptor protein 1 （TFR1）， and ferritin heavy chain 1 （FTH1）. ResultsCompared with that in the blank group， the survival rate of 4T1 cells in CuB groups was significantly decreased （P<0.05）， and the number of cell clones in CuB groups was significantly reduced （P<0.01）. In addition， compared with that in the blank group， the leakage of LDH in cells in CuB groups was significantly increased （P<0.01）， and the mitochondrial membrane potential of cells in CuB groups decreased significantly （P<0.01）. Cellular ROS levels were significantly elevated in CuB groups （P<0.01）. The mitochondria of cells in CuB groups were obviously wrinkled， and the mitochondrial cristae were reduced or even disappeared. Compared with that in the blank group， the protein expression of p53， ACSL4， and TFR1 were significantly up-regulated in CuB groups （P<0.05）， and that of SLC7A11， GPX4， and FTH1 were significantly down-regulated （P<0.05）. ConclusionCuB may inhibit SLC7A11 and GPX4 expression by up-regulating the expression of p53， which in turn regulates the p53/SLC7A11/GPX4 signaling pathway axis and accelerates the generation of lipid peroxidation substrate by up-regulating the expression of ACSL4. It up-regulates TFR1 expression to promote cellular uptake of Fe³⁺ and down-regulates the expression of FTH1 to reduce the ability of iron storage， resulting in an elevated free Fe²⁺ level. It catalyzes the Fenton reaction， generates excess ROS， imbalances the antioxidant system and iron metabolism， and then induces ferroptosis in 4T1 cells.

ObjectiveTo explore the role of cucurbitacin B （CuB） in inducing ferroptosis in 4T1 cells and its mechanism. MethodsThe effects of CuB（0.2， 0.4， 0.8 μmol·L^-1）on the proliferation ability of 4T1 cells in vitro were detected using the methyl thiazolyl tetrazolium （MTT） assay. The clonogenic ability of 4T1 cells was detected by the plate cloning assay， and the levels of lactate dehydrogenase （LDH） in 4T1 cells were detected by the use of a kit. The mitochondrial membrane potential and reactive oxygen species （ROS） levels in 4T1 cells were detected by flow cytometry， and the mitochondrial ultrastructure of 4T1 cells was observed by transmission electron microscopy. The western blot was used to detect the expression of ferroptosis-related protein p53 in 4T1 cells， solute carrier family 7 member 11 （SCL7A11）， glutathione peroxidase 4 （GPX4）， long-chain acyl-CoA synthetase 4 （ACSL4）， transferrin receptor protein 1 （TFR1）， and ferritin heavy chain 1 （FTH1）. ResultsCompared with that in the blank group， the survival rate of 4T1 cells in CuB groups was significantly decreased （P<0.05）， and the number of cell clones in CuB groups was significantly reduced （P<0.01）. In addition， compared with that in the blank group， the leakage of LDH in cells in CuB groups was significantly increased （P<0.01）， and the mitochondrial membrane potential of cells in CuB groups decreased significantly （P<0.01）. Cellular ROS levels were significantly elevated in CuB groups （P<0.01）. The mitochondria of cells in CuB groups were obviously wrinkled， and the mitochondrial cristae were reduced or even disappeared. Compared with that in the blank group， the protein expression of p53， ACSL4， and TFR1 were significantly up-regulated in CuB groups （P<0.05）， and that of SLC7A11， GPX4， and FTH1 were significantly down-regulated （P<0.05）. ConclusionCuB may inhibit SLC7A11 and GPX4 expression by up-regulating the expression of p53， which in turn regulates the p53/SLC7A11/GPX4 signaling pathway axis and accelerates the generation of lipid peroxidation substrate by up-regulating the expression of ACSL4. It up-regulates TFR1 expression to promote cellular uptake of Fe³⁺ and down-regulates the expression of FTH1 to reduce the ability of iron storage， resulting in an elevated free Fe²⁺ level. It catalyzes the Fenton reaction， generates excess ROS， imbalances the antioxidant system and iron metabolism， and then induces ferroptosis in 4T1 cells.

Objective:To screen and analyze the carcinogenesis-related differential expression profile of long non-coding RNAs(LncRNAs)in oral lichen planus(OLP)mucosa tissue,and preliminarily analyze their functions,to explore their possible role in the development of OLP.Methods:High-throughput sequencing technology was used to construct differential expression profile from 5 cases of erosive OLP lesions and 5 of normal oral mucosa.LncRNAs that are closely related to the carcinogenesis of OLP were ob-tained by bioinformatics analysis.Results:400 LncRNAs associated with OLP were screened,of which 250 were up-regulated and 150 were down-regulated,and 5 LncRNAs were obtained with differential expression associated with OLP carcinogenesis:LncRNA 54055,100128560,399717,378825 and 100130231.Conclusion:400 LncRNAs are differentially expressed in the mucosa of erosive OLP lesions,and 5 of them are related to the incidence and carcinogenesis tendency of OLP.

Objective:To explore the key components and mechanism of Qufeng Ningfei Powder in treating asthma through qualitative analysis of its blood components, combined with network pharmacology and molecular docking techniques.Methods:The blood components of Qufeng Ningfei Powder were qualitatively analyzed using UPLC-QE-Orbitrap-MS technology. R language was employed to analyze chip data from the GEO database, obtaining a list of differentially expressed genes. SwissTargetPrediction was utilized to predict the targets of drug components. Asthma-related targets were searched through databases such as OMIM, GeneCards, and TTD. The intersection of drug and disease targets was identified using Venn online analysis tool, constructing a "drug-component-target-disease" network to screen potential core components. A protein-protein interaction network (PPI) of core targets was constructed using STRING platform and Cytoscape software. GO function enrichment and KEGG pathway analysis were conducted using DAVID database to validate potential mechanism. Molecular docking was performed to verify the interaction between key components and core targets.Results:A total of 64 components were identified, from which 53 active components were screened, corresponding to 609 targets. Further searching disease databases revealed 96 target genes related to asthma, with an intersection of 6 genes between drug and asthma differential genes. Core target gene IL6 and its corresponding core compound were determined through network topology analysis. Molecular docking confirmed the binding of the main active components of Qufeng Ningfei Powder with the core target protein IL6.Conclusion:The blood components of Qufeng Ningfei Powder may regulate IL-17 through IL6, counteract airway remodeling, oxidative stress, and airway hyperresponsiveness, and thus treat asthma.

Objective:To screen and analyze the carcinogenesis-related differential expression profile of long non-coding RNAs(LncRNAs)in oral lichen planus(OLP)mucosa tissue,and preliminarily analyze their functions,to explore their possible role in the development of OLP.Methods:High-throughput sequencing technology was used to construct differential expression profile from 5 cases of erosive OLP lesions and 5 of normal oral mucosa.LncRNAs that are closely related to the carcinogenesis of OLP were ob-tained by bioinformatics analysis.Results:400 LncRNAs associated with OLP were screened,of which 250 were up-regulated and 150 were down-regulated,and 5 LncRNAs were obtained with differential expression associated with OLP carcinogenesis:LncRNA 54055,100128560,399717,378825 and 100130231.Conclusion:400 LncRNAs are differentially expressed in the mucosa of erosive OLP lesions,and 5 of them are related to the incidence and carcinogenesis tendency of OLP.

Development of new quality productive forces is an inherent requirement and a crucial focus for promoting high-quality development of public hospitals. Based on Marxist productivity theory, this study elucidated the essence of new quality productive forces in the health field and its correlation with high-quality development of public hospitals. By integrating innovative developmental practices of public hospitals in China, the practical problems of new quality productive forces in promoting high-quality development of public hospitals from three aspects(production factors, production technology, and production relations) were analyzed. Furthermore, corresponding development paths were proposed, including focusing on key production factors and consolidating the talent foundation of new quality productive forces, focusing on core production technologies and accumulating advantageous momentum to promote high-quality development, and focus on new production relations and coordinate the upgrading and growth of the health industry, to provide references for accelerating the high-quality development of public hospitals.

Objective·To investigate the changes of adipose tissues in mice after high-fat diet before and during pregnancy and the potential effects on adipose tissues in their offspring.Methods·C57BL/6J female mice were randomly assigned to the normal diet(CON group,n=12)or the high-fat diet(HFD group,n=12)for 5 weeks.The two groups were further subdivided according to pregnancy:a normal diet non-pregnancy group(CON-UN group),a normal diet pregnancy group(CON-P group),a high-fat diet non-pregnancy group(HFD-UN group),and a high-fat diet pregnancy group(HFD-P group).The original diet was maintained during pregnancy and lactation.White adipose tissues(WAT)and brown adipose tissues(BAT)were collected from visceral and scapula of mice after 5 weeks of feeding or E18.5d.Offspring from both dietary groups were placed on a normal diet after weaning,and their adipose tissues were collected at the 11th week.H-E staining was used to observe the changes of adipocytes.Flow cytometry was employed to detect the proportions of CD4+T cells,CD8+T cells,total T cells,CD4+T/CD8+T and NK cells in WAT.RT-PCR was used to assess the expression of IL-6 and IL-1β mRNA in WAT.Results·After 5 weeks on a high-fat diet,the body weight of female mice in the HFD group was higher than that in the CON group(P<0.05).Both WAT and BAT weights were markedly increased in the HFD groups before and during pregnancy(both P<0.05).In the WAT from HFD-UN and HFD-P groups,the number of cells within the same visual field decreased,the size of adipose cells varied,the proportion of fat droplets increased and the cell volume expanded.The proportion of lipid drop area to total visual field in the HFD-UN group and HFD-P group was compared with the CON-UN group and CON-P group,respectively,and the difference was statistically significant(all P<0.05).BAT in the HFD-UN and HFD-P groups showed a relatively chaotic arrangement and varying adipocyte sizes,although cell volume remained unchanged.The proportions of CD8+T cells and total T cells in adipose tissues were elevated in the HFD-UN and HFD-P groups,accompanied by increased mRNA levels of IL-6 and IL-1β,respectively,compared with the CON-UN and CON-P groups,and the differences were statistically significant(all P<0.05).NK cells proportions decreased at reproductive age(HFD-UN group)but increased significantly during pregnancy(HFD-P group),showing a divergent trend.Despite a return to a normal diet after weaning,offspring from the high-fat diet group had significantly higher weight of body,WAT and BAT,compared to those of normal diet(all P<0.05),and the volume of WAT was significantly enlarged.Conclusion·A high-fat diet can induce the changes of adipocyte structure and immune cell ratio,and elevate inflammation levels in adipose tissues before and during pregnancy,which also impacts the adipose structure in offspring.Adipose tissue may be a new vector mediating the intergenerational transmission of obesity.

Ferroptosis， a new form of programmed cell death different from apoptosis， necrosis， and autophagy， is closely associated with a variety of physiological and pathological processes. Iron-mediated accumulation of reactive oxygen species is the main inducement of ferroptosis， the mechanism of which is related to intracellular lipid metabolism， iron metabolism， and antioxidant defense pathways. Multiple signaling axes and regulators jointly regulate the occurrence and disruption of ferroptosis. Studies have demonstrated that ferroptosis regulates the growth and proliferation of tumor cells. Inducing ferroptosis in tumor cells can control the growth， metastasis， and multi-drug resistance of tumors. Therefore， the effect and mechanism of ferroptosis on tumor cells have become a hot topic in anti-cancer research. As the research advances， a variety of ferroptosis inducers has been used in the clinical chemotherapy for cancers and demonstrate significant efficacy. Accordingly， the development of ferroptosis-inducing anticancer drugs has become a new research direction for tumor treatment. Some active ingredients such as lycorine， oleanolic acid， dihydroartemisinin， pseudolaric acid B， and ophiopogonin B of Chinese medicines can induce ferroptosis in tumor cells via lipid metabolism， iron metabolism， system X_c^-， and GPX4/GSH to regulate the development of tumors， demonstrating a promising prospect in clinical treatment. Based on the theory of the mechanism of ferroptosis， this paper reviews the research progress in ferroptosis induced by active ingredients of Chinese medicines in tumor cells and describes the metabolic regulatory network of ferroptosis from signaling pathways and regulatory factors， providing new strategies for applying active ingredients of Chinese medicines in the treatment of tumors.

ObjectiveTo investigate the induction of ferroptosis by polyphyllin Ⅱ （PPⅡ） in hepatocellular carcinoma HepG2 cells and its underlying mechanism. MethodThe effect of PPⅡ （0， 1.5， 3.0， 4.5， 6.0， 9.0， 18.0 mg·L^-1） on the in vitro proliferation of HepG2 cells was assessed using the methyl thiazolyl tetrazolium （MTT） assay. Colony formation ability of HepG2 cells was evaluated through a colony formation assay. Cell migration ability was assessed via a scratch assay. Lactate dehydrogenase （LDH） content in HepG2 cells was measured using a kit. Reactive oxygen species （ROS） levels in HepG2 cells were observed using a fluorescence inverted microscope. Malondialdehyde （MDA）， glutathione （GSH）， and free Fe²⁺ content in HepG2 cells were detected using respective kits. The mitochondrial ultrastructure in HepG2 cells was observed by transmission electron microscopy. The expression of ferroptosis-related proteins p53， solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， long-chain acyl-CoA synthetase 4 （ACSL4）， and transferrin receptor 1 （TFR1） in HepG2 cells was detected using Western blot. ResultCompared with the control group， the PPⅡ treatment groups showed significantly decreased survival rate of HepG2 cells in a dose-dependent manner （P<0.01）， significantly reduced number of cell colonies （P<0.01）， significantly shortened scratch healing distance， inverse correlation of the migration distance with drug concentration （P<0.01）， significantly increased LDH leakage in cells （P<0.01）， significantly enhanced relative fluorescence intensity of intracellular ROS， and significantly increased accumulation of lipid peroxide MDA （P<0.01）， decreased intracellular GSH content with increasing drug concentration （P<0.01）， and significantly enhanced fluorescence intensity of FeRhoNox-1 in cells （P<0.01）. Moreover， cells exhibited vacuolation， and mitochondria showed significant shrinkage with reduced or even disappeared cristae. Compared with the results in the control group， the expression of p53， ACSL4， and TFR1 proteins significantly increased， while the expression of SLC7A11 and GPX4 proteins significantly decreased in the PPⅡ treatment groups （P<0.05）. ConclusionIn summary， PPⅡ induces ferroptosis in HepG2 cells by regulating the p53/SLC7A11/GPX4 signaling axis， promoting ACSL4 expression and Fe³⁺ uptake， leading to an imbalance in the antioxidant system.

It is of great significance to construct an information platform for performance appraisal of tertiary public hospitals to realize real-time monitoring and intervention of appraisal indicators, which is conducive to the transmission of responsibility for index optimization to departments and medical groups, and to promote the fine management of hospitals and promote high-quality development.This paper introduced the practice and effect of building a performance appraisal information platform for tertiary public hospitals in four aspects: accurate data filling, timely dynamic monitoring, visual display and safety management since 2022. At the same time, suggestions were put forward for platform optimization from four aspects: data quality control, co-construction and sharing, promotion and application, and system integration, in order to provide reference for other hospitals.