ObjectiveTo explore the mechanism of Sangpi Zhike prescription in treating cough after respiratory syncytial virus （RSV） infection through the "lung-intestine co-treatment" approach using network pharmacology and animal experimental validation. MethodsActive ingredients and targets of Sangpi Zhike prescription were retrieved from the Traditional Chinese Medicine Systems Pharmacology （TCMSP） database. Disease targets were obtained from GeneCards and Online Mendelian Inheritance in Man（OMIM） databases. Protein-protein interaction （PPI） networks and drug-component-target networks were constructed using overlapping targets between drugs and diseases to identify core targets. Gene ontology（GO） and Kyoto encyclopedia of genes and genomes（KEGG） pathway enrichment analyses were performed on the overlapping targets. Sixty mouse models were established： 10 as the normal group， and the remaining mice were infected with RSV via slow nasal drip of RSV suspension， with cough induced using capsaicin solution. After modeling， mice were divided into a model group， a Montelukast Sodium group （1 mg·kg^-1·d^-1）， and low， medium， and high dose groups of Sangpi Zhike prescription （4.875，9.75，and 19.5 g·kg^-1·d^-1）， with 10 mice per group. From day 14 after RSV infection， the normal and model groups received saline via gavage， while other groups received corresponding drug treatments once daily for 5 d. Hematoxylin-eosin（HE） staining was used to observe pathological changes in lung and intestinal tissue. The protein content of extracellular signal-regulated kinase 1/2 （ERK1/2） and phosphorylated （p）-ERK1/2 in the lung and colon tissue of mice was detected by Western blot. Real-time polymerase chain reaction（Real-time PCR） detected ERK1/2 mRNA expression in lung and intestinal tissue. Immunohistochemistry assessed p-MEK1/2， p-ERK1/2， p-c-Fos protein levels， and inflammatory cytokines interleukin（IL）-4 and （TNF）-α in lung and colon tissue. ResultsNetwork pharmacology identified 184 active ingredients and 684 targets in Sangpi Zhike prescription， with 1 344 RSV-related disease targets and 209 overlapping targets. Core targets included TNF， Fos， and Jun. KEGG enrichment revealed 179 pathways， primarily mitogen-activated protein kinase（MAPK）， cancer， TNF， and IL-17 signaling pathways. Animal experiments showed that， compared to those of the normal group， the lung tissue sections of the model group showed typical inflammatory damage， infiltration of inflammatory cells， rupture of alveolar septa， extensive alveolar fusion， and disruption of tight junctions between single-layer columnar epithelial cells in the intestinal tissue. The values of p-ERK1/2 and ERK1/2 in lung and intestinal tissue were significantly increased （P<0.01）， and the expression level of ERK1/2 mRNA was significantly elevated （P<0.01）. The levels of ERK1/2， p-MEK1/2， p-ERK1/2， p-c-Fos， IL-4， and TNF-α along the ERK pathway were significantly increased （P<0.05， P<0.01）. Compared to the model group， Sangpi Zhike prescription groups showed reduced lung and intestinal inflammation， decreased p-ERK1/2/ERK1/2 ratios （P<0.05，P<0.01）， lower ERK1/2 mRNA levels， and downregulated ERK pathway proteins （P<0.05，P<0.01）. ConclusionSangpi Zhike prescription alleviates cough and intestinal symptoms after RSV infection via the "lung-intestine co-treatment" mechanism by suppressing expression levels of ERK1/2， p-MEK1/2， p-ERK1/2， p-c-Fos， IL-4， and TNF-α on ERK pathway components， thereby mitigating lung and intestinal pathological damage.

Diabetic nephropathy （DKD）， as a common microvascular complication of diabetes mellitus （DM）， is a major cause of end-stage renal disease （ESRD）. Its clinical manifestations include increased urinary protein excretion， thickening of the glomerular basement membrane， and renal tubulointerstitial fibrosis. The pathogenesis of DKD is complex and involves multiple factors， including disordered glucose metabolism， hemodynamic alterations， and oxidative stress. Although modern medical approaches can alleviate certain symptoms， they still have limitations such as insufficient therapeutic targeting and prominent adverse effects. The transforming growth factor-β/Smad （TGF-β/Smad） signaling pathway is not only a tissue fibrosis pathway that has attracted considerable attention in recent years， but also regulates multiple protein molecules， including the glomerular podocyte slit diaphragm protein Podocin， interleukin-1β （IL-1β）， and superoxide dismutase （SOD）， thereby participating in various pathological processes and ultimately mediating renal injury. Flavonoid compounds， owing to their sustained pharmacological effects， broad spectrum of action， and high safety profile， have become ideal candidates for targeted therapy research in DKD. Existing studies have shown that these compounds can exert inhibitory effects on renal fibrosis， alleviate inflammatory responses， protect podocytes， and reduce oxidative stress by regulating the interactions between the TGF-β/Smad signaling pathway and the aforementioned protein molecules， thereby maintaining renal structure and function， reducing proteinuria， and significantly improving DKD lesions. This review briefly outlines the composition and functions of the TGF-β/Smad signaling pathway， elucidates the mechanisms by which this pathway regulates DKD， and focuses on summarizing major studies from the past decade on flavonoid-based interventions in DKD through targeted inhibition of the TGF-β/Smad signaling pathway. Furthermore， it discusses the considerable therapeutic potential of flavonoids in the treatment of this disease， aiming to provide a scientific basis for future clinical prevention and treatment of DKD and to promote the development of targeted drugs.

Hepatic ischemia-reperfusion injury(IRI)is a pathological phenomenon that commonly occurs during liver surgery and transplantation.It leads to serious tissue damage and affects liver function.The mechanisms behind IRI are complex,involving oxida-tive stress,inflammatory responses,and calcium homeostasis disorder.Recently,scientists have paid more attention to the role of endo-plasmic reticulum stress(ERS)in IRI.ERS activates three classical signaling pathways,PERK,IRE1,and ATF6,through the unfolded protein response(UPR),aiming to preliminarily restore endoplasmic reticulum homeostasis and protect cells.However,if the stress re-sponse is excessive or persistent,ERS can activate apoptosis signaling pathways,such as CHOP and Bax/Bak,worsening cell injury.Additionally,ERS is closely related to other cellular stress responses,such as autophagy and oxidative stress,which jointly affect the survival and death of hepatocytes.Regulation of ERS,especially interventions targeting the three UPR pathways,is considered as a po-tential therapeutic pathway for alleviating hepatic IRI.Pharmacological interventions,such as 4-phenylbutyric acid and taurocholic acid,and gene therapies,such as knocking out PERK or IRE1,have shown positive effects in protecting liver function while inhibiting ERS.This paper reviews the mechanism of action of ERS in hepatic IRI,focuses on the specific roles of the three UPR pathways and their potential as therapeutic targets,and explores the future of re-lated therapeutic strategies.

Laboratory animals are the "living" tools of medical research. Through animal experiments, people can gain continuous insights into the laws of life, reveal the essence of diseases, develop vaccines and drugs for prevention and treatment, and play an important role in the technological development of fields related to human health. The environmental conditions of laboratory animals have a direct impact on their health, quality, and the results of animal experiments. The higher the degree of environmental control, the more reliable the experimental results are in terms of quality. Therefore, environmental control of laboratory animal facilities is important for ensuring that laboratory animals live under required conditions, which is a key factor for conducting effective animal experiments. This article analyzes the current status of environmental testing of laboratory animal facilities in Sichuan Province, briefly summarizing their number, area, and other basic information, and provides detailed statistics on the ability of institutions to conduct environmental testing for laboratory animal facilities in Sichuan Province. It also summarizes the testing requirements for laboratory animal facility environments based on national standards, regulatory requirements, and the quality control needs of facility users. In the analysis of testing indicators for laboratory animal facilities, based on testing data from 40 laboratory animal facilities in Sichuan Province, it was found that static pressure difference is the indicator most prone to non-compliance, followed by illumination and air exchange rate. Using barrier environments as examples, common problems in the process of environmental testing for laboratory animal facilities are summarized in six aspects: testing personnel, instruments, methods, technical materials, testing environment, and reports, and targeted suggestions are proposed. These suggestions help improve environmental control in laboratory animal facilities, and provide practical reference and guidance for relevant testing institutions, as well as laboratory animal producers and users in the industry.

Objective To investigate the inhibitory effect of Scutellaria baicalensis combined with 5-Fu on Lewis tumor bearing mouse lung cancer based on the JAK2/STAT3 signaling pathway.Methods To detect the changes in body mass,food intake and tumor volume of Lewis tumor-bearing mice after intervention of Scutellaria baicalensis(20 mg/kg)combined with 5-Fu.Pathological changes in tumor tissue were observed by HE staining,expression levels of proliferation related protein Ki67 were observed by immunohistochemical staining,changes in cell apoptosis levels in tumor tissue were observed by TUNEL staining,and changes in expression levels of JAK2,p-JAK2,STAT3,and p-STAT3 proteins in tumor tissue were observed by immunohistochemical staining.Results Compared with the model group,the tumor volume of mice after combined intervention significantly decreased(P＜0.01)and body mass increased(P＜0.05),but there was no significant change food intake.The expression of proliferation related protein Ki67 in tumor tissue was significantly reduced,and the number of apoptotic cells labeled with TUNEL was significantly increased;The expression of p-JAK2 and p-STAT3 proteins is elevated.Conclusions Scutellaria baicalensis decoction can inhibit the JAK2/STAT3 signaling pathway and increase the inhibitory effect of 5-Fu on mouse lung cancer.

Cognitive dysfunction is a common complication of diabetes mellitus(DM)with a complex pathogenesis that may be closely related to neuropathic changes.Functional magnetic resonance imaging(fMRI)can investigate brain function by measuring changes in brain tissue structure and hemodynamics following enhanced neural activity,potentially facilitating early detection of the brain pathophysiological changes underlying cognitive dysfunction in DM.This paper reviews the application of fMRI technology in the assessment of brain structure and function in diabetic patients,aiming to provide a basis for the early detection,intervention,and research on cognitive impairment in DM.

Cognitive dysfunction is a common complication of diabetes mellitus(DM)with a complex pathogenesis that may be closely related to neuropathic changes.Functional magnetic resonance imaging(fMRI)can investigate brain function by measuring changes in brain tissue structure and hemodynamics following enhanced neural activity,potentially facilitating early detection of the brain pathophysiological changes underlying cognitive dysfunction in DM.This paper reviews the application of fMRI technology in the assessment of brain structure and function in diabetic patients,aiming to provide a basis for the early detection,intervention,and research on cognitive impairment in DM.

Objective To investigate the inhibitory effect of Scutellaria baicalensis combined with 5-Fu on Lewis tumor bearing mouse lung cancer based on the JAK2/STAT3 signaling pathway.Methods To detect the changes in body mass,food intake and tumor volume of Lewis tumor-bearing mice after intervention of Scutellaria baicalensis(20 mg/kg)combined with 5-Fu.Pathological changes in tumor tissue were observed by HE staining,expression levels of proliferation related protein Ki67 were observed by immunohistochemical staining,changes in cell apoptosis levels in tumor tissue were observed by TUNEL staining,and changes in expression levels of JAK2,p-JAK2,STAT3,and p-STAT3 proteins in tumor tissue were observed by immunohistochemical staining.Results Compared with the model group,the tumor volume of mice after combined intervention significantly decreased(P＜0.01)and body mass increased(P＜0.05),but there was no significant change food intake.The expression of proliferation related protein Ki67 in tumor tissue was significantly reduced,and the number of apoptotic cells labeled with TUNEL was significantly increased;The expression of p-JAK2 and p-STAT3 proteins is elevated.Conclusions Scutellaria baicalensis decoction can inhibit the JAK2/STAT3 signaling pathway and increase the inhibitory effect of 5-Fu on mouse lung cancer.

Objective To investigate the effect of E2 signaling in myofibers on muscular macrophage efferocytosis in mice with cardiotoxin-induced acute skeletal muscle injury.Methods Female wild-type C57BL/6 mice with and without ovariectomy and male C57BL/6 mice were given a CTX injection into the anterior tibial muscle to induce acute muscle injury,followed by intramuscular injection of β-estradiol(E2)or 4-hydroxytamoxifen(4-OHT).The changes in serum E2 of the mice were detected using ELISA,and the number,phenotypes,and efferocytosis of the macrophages in the inflammatory exudates and myofiber regeneration and repair were evaluated using immunofluorescence staining and flow cytometry.C2C12 cells were induced to differentiate into mature myotubes,which were treated with IFN-γ for 24 before treatment with β-Estradiol or 4-OHT.The treated myotubes were co-cultured with mouse peritoneal macrophages in a 1:2 ratio,followed by addition of PKH67-labeled apoptotic mouse mononuclear spleen cells induced by UV irradiation,and macrophage efferocytosis was observed using immunofluorescence staining and flow cytometry.Results Compared with the control mice,the female mice with ovariectomy showed significantly increased mononuclear macrophages in the inflammatory exudates,with increased M1 cell percentage,reduced M2 cell percentage and macrophage efferocytosis in the injured muscle,and obviously delayed myofiber regeneration and repair.In the cell co-culture systems,treatment of the myotubes with β-estradiol significantly increased the number and proportion of M2 macrophages and macrophage efferocytosis,while 4-OHT treatment resulted in the opposite changes.Conclusion In injured mouse skeletal muscles,myofiber E2 signaling promotes M1 to M2 transition to increase macrophage efferocytosis,thereby relieving inflammation and promoting muscle regeneration and repair.

Peripheral arterial disease is one of the common complications of diabetes. At present, the pathogenesis of diabetic peripheral arterial diseases is not completely clear, and there is a lack of effective treatment methods and drugs. Adipokines have profound impact on the occurrence and development of diabetes mellitus and its complications, and are directly or indirectly involved in the progression of diabetic peripheral arterial diseases. Different adipokines may inhibit or promote the occurrence of vascular diseases with the mechanisms that are complex and controversial. Adipokines are expected to be a new target for the treatment of diabetic peripheral arterial disease, which is worthy of further study. This article mainly reviews the relationship between some common adipokines and new adipokines and diabetic vascular disease, aiming to provide new methods for the clinical treatment of diabetic peripheral arterial disease.