ObjectiveTo investigate the mechanisms of Tongnao decoction （TND） in mice with acute ischemic stroke （AIS）. MethodsFifty male C57BL/6J mice were randomly divided into a sham operation group， model group， TND low-dose group （1.86 g·kg^-1）， TND high-dose group （3.72 g·kg^-1）， and butylphthalide （NBP） group （10 mg·kg^-1）， with 10 mice in each group. A mouse model of cerebral ischemic injury was established using photochemical thrombosis （PT）. The sham operation group and model group were administered an equal volume of normal saline by gavage. All five groups were treated once daily for 14 consecutive days. Behavioral tests were performed before modeling and at the end of administration. T₂-weighted imaging （T₂WI） was performed 3 days after modeling to evaluate the extent of injury. Hematoxylin-eosin （HE） staining was used to observe histological changes in the cerebral cortex， and Nissl staining was used to observe neuronal morphology. Cerebral blood flow in mice was detected using a laser speckle contrast imaging （LSCI） system. Immunofluorescence staining was used to detect the cell proliferation marker bromodeoxyuridine （BrdU） and the highly glycosylated type I transmembrane glycoprotein CD34. Western blot analysis was used to detect the expression levels of phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， glycogen synthase kinase-3β （GSK-3β）， and their phosphorylation levels， as well as tight junction-related proteins zonula occludens-1 （ZO-1）， Occludin， and Claudin-5 in the peri-infarct tissue. Thirty-five zebrafish were randomly divided into normal control group， model group， TND low and high dose groups （0.16， 0.32 g·L^-1） and NBP group （10 μmol·L^-1）， with 7 in each group. A stereoscopic fluorescence microscope was used to observe vascular growth in zebrafish. ResultsImaging showed that PT caused ischemia in the right cortical region. Behavioral tests indicated that， compared with the model group， the drug-treated groups reduced the error rate of irregular balance ladder climbing on the affected side and shortened the tape removal time （P<0.05）. HE staining and Nissl staining showed that， compared with the model group， the drug-treated groups exhibited reduced brain tissue damage， fewer scars， and improved neuronal morphology. LSCI results showed that the drug-treated groups partially restored cerebral blood perfusion and promoted the establishment of collateral circulation compared with the model group. Immunofluorescence staining indicated that the drug-treated groups increased the positive rates of BrdU and CD34 compared with the model group （P<0.01）， promoting angiogenesis. Meanwhile， compared with the model group， the drug-treated groups upregulated the expression levels of p-PI3K， p-Akt， p-GSK-3β， and tight junction proteins ZO-1， Occludin， and Claudin-5 （P<0.05，P<0.01）， and increased the number of intersegmental vessels in zebrafish （P<0.05，P<0.01）. ConclusionTND can promote angiogenesis around the infarct in PT model mice by regulating the PI3K/Akt/GSK-3β signaling pathway， thereby improving cerebral ischemic injury.

OBJECTIVE To provide references and suggestions for the establishment of medication management in care transitions in China. METHODS This study systematically reviewed the medication management in care transitions led by pharmacists in the United States， summarized the clinical practice evidence of its service system， personnel configuration， development bottlenecks and effect benefits， and explored the suggestions for optimizing the work in China. RESULTS & CONCLUSIONS The United States medication management in care transitions is characterized by standardized workflows and precision interventions. It focuses on the treatment continuity period when patients transition across institutions and stages， establishing a pharmacist-led， multidisciplinary collaborative monitoring system. Empirical studies confirm its effectiveness in reducing medication errors， lowering healthcare costs， and improving patient satisfaction. The United States model has achieved professionalization and standardization. Adapting its successful experiences as well as combining our local situation can establish a pharmacist-led medication management framework in care transitions through four key dimensions： role definition， training mechanisms， standardized protocols， and evaluation metrics， and improve the further development of pharmaceutical care services.

ObjectiveTo explore the mechanism of Yishen Qubi Tongluo Formula （益肾祛痹通络方， YQTF） in the treatment of rheumatoid arthritis（RA）. MethodsNetwork pharmacology was employed to retrieve and screen the active components and potential targets of YQTF as well as RA-related targets using databases including TCMSP， BATMAN， ETCM and GEO. The intersection of targets related to active components and RA-related targets was identified， and a protein-protein interaction （PPI） network was constructed. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed， and a drug-active component-common target network of YQTF in the treatment of RA was established. The core components of YQTF were molecularly docked with key targets. Human rheumatoid arthritis synovial fibroblast cell line MH7A was divided into blank group， model group， methotrexate group and YQTF group. The blank group was cultured with 10% fetal bovine serum， while the other three groups were stimulated with 10 μg/L of recombinant human tumor necrosis factor-α （TNF-α） for 24 h to establish the RA cell model. On this basis， the methotrexate group was treated with methotrexate suspension at a concentration of 20 μmol/L， and the YQTF group was treated with 10% YQTF-medicated serum. After 48 h of intervention， the levels of TNF-α and interleukin-17A（IL-17A）contents in cell supernatants were detected by enzyme-linked immunosorbent assay （ELISA）， and mRNA expressions of phosphatidylinositol 3-kinase（PI3K）， protein kinase B（AKT） and mammalian target of rapamycin（mTOR） were detected by real-time quantitative polymerase chain reaction （RT-qPCR）. ResultsNetwork pharmacological analysis identified 209 active components and 583 potential target genes of YQTF， as well as 818 RA-related targets. A total of 29 common targets were obtained from the intersection of drug-related targets and RA-related targets. Quercetin，β-sitosterol， kaempferol， stigmasterol and luteolin were the core active components of YQTF for the treatment of RA， while matrix metalloproteinase-9 （MMP9）， prostaglandin-endoperoxide synthase 2 （PTGS2）， Toll-like receptor 4 （TLR4）， tumor protein p53 （TP53） and transcription factor AP-1 subunit JUN were the key targets. The GO and KEGG pathway enrichment analysis showed that the involved biological processes and pathways were mainly associated with antioxidant responses， PI3K-AKT signaling pathway and Toll-like receptor （TLR） signaling pathway. Molecular docking results showed that MMP9 and PTGS2 exhibited high binding affinities with quercetin， β-sitosterol， kaempferol， stigmasterol and luteolin； TLR4 exhibited high binding activities with β-sitosterol， stigmasterol and luteolin； and TP53 showed high binding affinity with luteolin. The results of cell experiments showed that compared with the control group， the contents of TNF-α and IL-17A as well as the mRNA expressions of AKT and mTOR in the model group significantly increased （P＜0.05 or P＜0.01）. Compared with the model group， all the above indicators significantly decreased in the YQTF group， while the contents of TNF-α and the mRNA expression of AKT significantly decreased in the methotrexate group （P＜0.05 or P＜0.01）. ConclusionThe mechanism of YQTF in the treatment of RA may be associated with reducing inflammatory cytokine secretion and inhibiting the activation of the PI3K-AKT-mTOR signaling pathway.

ObjectiveTo explore the effect of the medical-community linkage model on activities of daily living, psychological status and motor function of stroke patients in the community. MethodsA total of 60 stroke patients admitted to two community health service centers and their affiliated stations in Fengtai District, Beijing, from January, 2024 to August, 2025 were enrolled and randomly divided into control group (n = 30) and intervention group (n = 30). The control group received routine medicine, dietary care and rehabilitation management, while the intervention group underwent rehabilitation with the medical-community linkage model, for twelve weeks. They were assessed with modified Barthel Index (MBI), Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD) and Fugl-Meyer Assessment (FMA) before and after intervention. ResultsAfter intervention, the MBI, HAMA, HAMD and FMA scores of patients improved in both groups (|t| > 5.599, P < 0.001), and improved more in the intervention group than in the control group (P < 0.05), except MBI. The HAMA and HAMD scores of family members decreased in both groups (|t| > 10.333, P < 0.001), and decreased more in the intervention group than in the control group (t > 5.681, P < 0.001). ConclusionThe medical-community linkage model can further improve the motor function of stroke patients in community, as well as the psychological status of both patients and their family members.

ObjectiveThis study aimed to investigate the anti-Mycoplasma pneumoniae (MP) activity of luteolin and elucidate its underlying mechanisms. MethodsLuteolin was identified as the primary active compound from the polyphenol extract ofF. diotrys using network pharmacology. Its efficacy was evaluated against two MP strains: the standard strain M129 and the multidrug-resistant strain M19. A modified culture medium with visual characteristics was employed to determine the minimum inhibitory concentration (MIC) of luteolin. The expression of key proteins involved in MP growth and pathogenicity was assessed by qRT-PCR following luteolin treatment. Additionally, the viability of A549 cells infected with MP was compared between luteolin-treated and untreated groups. In vivo anti-MP activity was evaluated using a mouse model, and the expression of inflammatory cytokines in lung tissues was analyzed. ResultsLuteolin effectively inhibited both MP strains, with MIC₉₀ values of 100 mg/L for M19 and M129. Treatment with luteolin significantly downregulated the expression of adhesion proteins P1 and P30 in both strains. However, the expression of P65, HMW3, TrmB, and CARDS TX was reduced only in the M19 strain following luteolin intervention. Luteolin also enhanced the growth and viability of A549 cells infected with MP. In the mouse model, luteolin treatment resulted in steady weight gain and was well tolerated. The bacteriostatic rate of luteolin in lung tissues was 50.7%, significantly higher than the 25.2% observed in the roxithromycin group. Furthermore, luteolin reduced the expression of inflammatory factors, including IL-6, TNF-α, and HMGB1, in MP-infected mice. ConclusionLuteolin effectively and safely inhibits the proliferation and pathogenicity of MP, particularly the drug-resistant M19 strain, by downregulating the expression of toxicity-associated proteins (P1, P30, P65, HMW3, TrmB, CARDS TX) and modulating host inflammatory responses. These findings suggest that luteolin may offer a novel therapeutic strategy for treating MP infections, especially those caused by drug-resistant strains.

ObjectiveTo investigate the contamination status of ochratoxin A (OTA) in commercially available food products in Shanghai, and to assess OTA exposure levels and the associated non-carcinogenic and carcinogenic risks among pregnant women by integrating dietary consumption data of this population. MethodsThe levels of OTA contamination in 1 520 food samples collected in Shanghai from 2022 to 2023 were determined using liquid chromatography-tandem mass spectrometry. An exposure assessment model was developed based on the dietary consumption levels of pregnant women from the 2016‒2017 Shanghai Pregnant Women Dietary Monitoring Survey to calculate the estimated daily intake (EDI) of OTA, the margin of exposure for non-carcinogenic toxicity (MOE₁), and the margin of exposure for carcinogenic toxicity (MOE₂). An MOE₁ greater than 200 and an MOE₂ greater than 10 000 indicate that the non-carcinogenic toxicity and carcinogenic toxicity resulting from exposure are negligible, respectively. For samples with OTA contamination levels below the limit of detection (LOD), which accounted for more than 80% of the samples, the OTA levels were assigned values of 0 and LOD, respectively, for subsequent calculations. ResultsThe detection rates of OTA in cereals, nuts, dried fruits, and alcohol samples collected in 2022 were 2.03%, 0, 0, and 0, respectively. The OTA detection rates in cereals, nuts, dried fruits, beans, and alcohol samples collected in 2023 were 2.50%, 0.39%, 2.47%, 1.67%, and 13.33%, respectively. For pregnant women in Shanghai in 2022, simulation results indicated that when assigning a value of 0 and the LOD, theP₅₀ values of EDI for dietary OTA exposure were 0.05 and 0.72 ng·(kg·d)^-1, respectively, and the P₉₅ values of EDI for dietary OTA exposure were 0.25 and 2.40 ng·(kg·d)^-1, respectively. For pregnant women in Shanghai in 2023, the P₅₀ values of EDI for dietary OTA exposure were 0.04 and 1.00 ng·(kg·d)^-1, respectively, and the P₉₅ values of EDI for dietary OTA exposure were 0.23 and 2.67 ng·(kg·d)^-1, respectively, both substantially below the tolerable daily intake (TDI) for OTA [17 ng·(kg·d)^-1]. The EDI for dietary OTA exposure in 100.0% of Shanghai pregnant women was lower than the TDI, indicating an overall low level of dietary OTA exposure among this population. For 100.0% of pregnant women, the MOE₁ for dietary OTA exposure exceeded 200. When assigned a value of 0, the MOE₂ for 100.0% of pregnant women in both 2022 and 2023 exceeded10 000. When assigned the LOD value, 72.3% and 81.8% of pregnant women in 2022 and 2023, respectively, had an MOE₂ exceeding 10 000. ConclusionFrom 2022 to 2023, samples of cereals, nuts, dried fruits, beans, and alcohol sold in Shanghai exhibited varying degrees of OTA contamination. The overall EDI of OTA exposure among pregnant women in Shanghai remained at a low level. The non-carcinogenic and carcinogenic risks associated with OTA exposure were generally low and at controllable levels.

ObjectiveThis study aimed to investigate the anti-Mycoplasma pneumoniae (MP) activity of luteolin and elucidate its underlying mechanisms. MethodsLuteolin was identified as the primary active compound from the polyphenol extract ofF. diotrys using network pharmacology. Its efficacy was evaluated against two MP strains: the standard strain M129 and the multidrug-resistant strain M19. A modified culture medium with visual characteristics was employed to determine the minimum inhibitory concentration (MIC) of luteolin. The expression of key proteins involved in MP growth and pathogenicity was assessed by qRT-PCR following luteolin treatment. Additionally, the viability of A549 cells infected with MP was compared between luteolin-treated and untreated groups. In vivo anti-MP activity was evaluated using a mouse model, and the expression of inflammatory cytokines in lung tissues was analyzed. ResultsLuteolin effectively inhibited both MP strains, with MIC₉₀ values of 100 mg/L for M19 and M129. Treatment with luteolin significantly downregulated the expression of adhesion proteins P1 and P30 in both strains. However, the expression of P65, HMW3, TrmB, and CARDS TX was reduced only in the M19 strain following luteolin intervention. Luteolin also enhanced the growth and viability of A549 cells infected with MP. In the mouse model, luteolin treatment resulted in steady weight gain and was well tolerated. The bacteriostatic rate of luteolin in lung tissues was 50.7%, significantly higher than the 25.2% observed in the roxithromycin group. Furthermore, luteolin reduced the expression of inflammatory factors, including IL-6, TNF-α, and HMGB1, in MP-infected mice. ConclusionLuteolin effectively and safely inhibits the proliferation and pathogenicity of MP, particularly the drug-resistant M19 strain, by downregulating the expression of toxicity-associated proteins (P1, P30, P65, HMW3, TrmB, CARDS TX) and modulating host inflammatory responses. These findings suggest that luteolin may offer a novel therapeutic strategy for treating MP infections, especially those caused by drug-resistant strains.

ObjectiveThis paper aims to investigate the mechanism by which Erchentang improves body weight in obese mice by regulating the AMP‑activated protein kinase （AMPK）/peroxisome proliferator‑activated receptor γ coactivator‑1α （PGC‑1α） signaling pathway and inducing browning of inguinal white adipose tissue （iWAT）. MethodsObese mouse models were established by feeding a high‑fat diet. After successful modeling， mice were randomly divided into a model group and low‑， medium‑， and high‑dose Erchentang groups （7.5， 15， 30 g·kg^-1）， with six mice in each group. Another six normal mice were set as the normal group. Mice in the treatment groups were administered with corresponding doses of the drug by gavage， while those in the normal and model groups were administered with an equal volume of pure water by gavage for four consecutive weeks. Obesity was evaluated by body weight and Lee's index. The levels of low‑density lipoprotein cholesterol （LDL‑C） and high‑density lipoprotein cholesterol （HDL‑C） in serum were detected by biochemical assays. The leptin content in serum was measured by enzyme‑linked immunosorbent assay （ELISA）. Hematoxylin and eosin （HE） staining was used to observe the pathological morphology of the liver and iWAT. Immunofluorescence staining was applied to detect the protein expression levels of glucose transporter 4 （GLUT4） in the liver and iWAT. Molecular docking was performed to simulate the binding affinity between the key components of Erchentang （nobiletin， diosmetin， naringenin） and the key pathway proteins AMPK and PGC‑1α. Western blot was used to detect the protein expression levels of uncoupling protein‑1 （UCP‑1）， AMPK， phosphorylated AMP-activated protein kinase （p‑AMPK）， and PGC‑1α in iWAT. ResultsCompared with those in the normal group， the mice in the model group showed significantly increased body weight and Lee's index， elevated levels of HDL‑C， LDL‑C， and leptin in serum， enlarged adipocytes in iWAT， down‑regulated protein expression levels of GLUT4 in iWAT and liver， and decreased protein expression levels of UCP‑1 and PGC‑1α in iWAT（P<0.05， P<0.01）， the expression level of p-AMPK / AMPK protein was up-regulated， but the difference was not statistically significant. Compared with those in the model group， the mice in the Erchentang groups with different doses exhibited significantly reduced body weight and Lee's index， decreased levels of HDL‑C， LDL‑C， and leptin in serum， smaller adipocytes in iWAT， up‑regulated GLUT4 protein expression levels in iWAT and liver， and increased protein expression levels of UCP‑1， p‑AMPK/AMPK， and PGC‑1α in iWAT （P<0.05， P<0.01）. Molecular docking results show that nobiletin， diosmetin， and naringenin have strong binding energies with both AMPK and PGC‑1α. ConclusionErchentang may improve body weight in obese mice by regulating the AMPK/PGC‑1α signaling pathway and inducing iWAT browning.

Hepatocellular carcinoma （HCC）， a malignancy with high mortality， exhibits poor survival rates and prognosis. The profound suppression of the tumor immune microenvironment （TIME） and the abnormal hyperactivity of metabolic reprogramming （MR） are the two primary factors driving HCC progression. Traditional Chinese medicine has demonstrated significant efficacy in HCC treatment. The team proposed that "deficiency of healthy Qi and stasis toxins" was the core pathogenesis of HCC， closely associated with TIME suppression and MR hyperactivity. This paper proposed that a suppressed state of the TIME was the biological manifestation of "deficiency of healthy Qi"， where the functional exhaustion of effector T lymphocytes and natural killer cells reflected the decline of "healthy Qi" in eliminating pathogens. Conversely， the expansion and activation of immunosuppressive cells， such as regulatory T cells （Tregs）， M2-like tumor-associated macrophages （TAM-M2）， and myeloid-derived suppressor cells （MDSCs） ， represent the dysfunction of "healthy Qi" in maintaining homeostasis. MR serves as the material basis of "stasis toxins". Stasis toxins exhibit heat stagnation， manifested by abnormal hyperactivity of glycolysis and lipid synthesis. They demonstrate migratory propensity， as toxic metabolites like lactic acid and prostaglandin E2 promote tumor invasion and metastasis. They display a consumptive nature， reflected in the functional suppression of immune cells. The vicious cycle between TIME and MR is the biopathological reflection of "deficiency of healthy Qi intertwined with stasis toxins". Immunosuppression exacerbates MR， while toxic metabolites further impair immune function， establishing a pathogenic chain of "deficiency leading to stasis， and stasis toxins damaging healthy Qi". The primary therapeutic approach is reinforcing healthy Qi， resolving stasis， and removing toxins， which can reinforce and tonify healthy Qi to regulate pathways， such as phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt）， C-X-C chemokine receptor type 4/ C-X-C chemokine ligand 12 （CXCR4/CXCL12）， and toll-like receptor 4/ nuclear factor-kappa B/ signal transducer and activator of transcription 3 （TLR4/NF-κB/STAT3）， adjust T lymphocyte ratios， inhibit Tregs/TAM-M2 function， and downregulate immune checkpoints， including programmed death ligand 1/programmed death 1（PD-L1/PD-1）， and reshape TIME. It is also involved in resolving stasis and removing toxins to modulate phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） and hypoxia-inducible factor-1α （HIF-1α） signaling pathways， suppress key enzymes in glycolysis and lipid synthesis， and block toxic metabolite production. Thus， this therapy synergistically regulates the immune and metabolic network， breaks the vicious cycle of "deficiency in healthy Qi and stasis toxins"， and offers a novel strategy for integrating traditional Chinese medicine and Western medicine in HCC treatment.

At present,the drug substitutes represented by new psychoactive substances are gradually be-coming popular,leading to an increasing demand for identifying novel drugs with unknown structures in drug investigation.Nuclear magnetic resonance(NMR)spectroscopy is an important tool for ana-lyzing molecular structures.In the absence of standard substances,quantitative NMR(qNMR)can un-dertake the quantitative analysis of target substances in complex mixtures and has unique advantages in the research of new drugs and their precursor drugs.Due to the limitations of the site and mainte-nance costs,as well as relatively complex operation,high-field superconducting NMR is less com-monly applied in drug research.The desktop low-field NMR developed in recent years provides a new alternative solution.Due to the use of permanent magnets,its size is reduced,and the operation and maintenance costs are lowered.It has been widely used in various research fields.This article reviews the development of low-field NMR technology,summarizes the application of desktop low-field NMR in screening and identification of suspicious substances,rapid content determination,analysis of drug manufacturing processes and synthetic routes,and correlation traceability.It also looks forward to the prospects and development directions of this technology in drug research,aiming to provide a reference for researchers who work in analytical chemistry and drug research.