Sepsis is a life-threatening organ dysfunction caused by infection-induced dysregulation of the host response. Its pathological mechanism is complex, involving excessive inflammatory response, immunosuppression and oxidative stress. Current clinical treatments mainly rely on anti-infection and supportive strategies, but the therapeutic efficacy is limited and the mortality remains high. Traditional Chinese medicine (TCM) monomers show great potential in sepsis treatment due to their multi-target, anti-inflammatory, antioxidant and immunomodulatory properties. Nevertheless, their clinical application is restricted by poor water solubility, low bioavailability and weak targeting ability. As an emerging nanoscale porous material, metal-organic frameworks (MOFs) have become ideal drug delivery carriers for their tunable pore size, high specific surface area and good biocompatibility. This review systematically elaborates the core advantages and mechanisms of MOFs as targeted drug delivery.

Sudden respiratory infectious diseases spread rapidly and pose significant challenges for prevention and control, representing a major public health concern globally. Xinjiang is rich in ethnic medical resources, with traditional medicinal materials such as Uyghur and Kazakh herbs demonstrating unique potential in antiviral, anti-inflammatory, antimicrobial, and immunomodulatory effects. This article reviews the chemical components, pharmacological effects and applications in respiratory infectious diseases of characteristic Xinjiang medicinal materials such as Fomes officinalis, Hyssopus officinalis, and Artemisia rupestris, as well as commonly used clinical preparations. Studies have found that ethnic medicinal materials and preparations exhibit synergistic mechanisms involving multiple components, targets, and pathways, which inhibit viral replication, modulate immune responses and mitigate inflammatory damage. They have demonstrated favorable efficacy and safety in clinical practice. This review further discusses the challenges faced in modernization, formulation optimization, and clinical validation of Xinjiang ethnic medicines, aiming to provide new medicinal resources and prevention strategies for addressing sudden respiratory infectious diseases.

The study employed a serum pharmacology approach to investigate the mechanism by which the blood-absorbed components of Dengzhan Shengmai Formula (DZSM) promote angiogenesis in mouse brain microvascular endothelial cells (bEND.3) following oxygen-glucose deprivation/reoxygenation (OGD/R) injury. The blood-absorbed constituents of DZSM were identified using ultra-high performance liquid chromatography coupled with quadrupole electrostatic field orbitrap high-resolution mass spectrometry (UHPLC-Q-Exactive-Orbitrap). An OGD/R-injured bEND.3 cell model was established. Cell viability was measured by CCK-8 assay, cellular injury was assessed by lactate dehydrogenase (LDH) levels, reactive oxygen species (ROS) expression was detected by confocal microscopy, and the apoptosis rate was determined by flow cytometry. The pro-angiogenic effect of DZSM-medicated serum was evaluated through wound healing assay, Transwell migration assay, tube formation assay, transepithelial electrical resistance (TEER), and NaF permeability test. Protein expression related to the hypoxia inducible factor-1/vascular endothelial growth factor A (HIF-1α/VEGFA) signaling pathway was detected by Western blot, and molecular docking was performed to screen key active components. The results showed that twelve components, including scutellarin, 4, 5-dicaffeoylquinic acid, and ginsenoside Rb2, were absorbed into the blood. The optimal concentration of DZSM-medicated serum for intervening in OGD/R-injured bEND.3 cells was 20% (v/v). Compared with the control group, the model group exhibited significantly decreased cell viability, migration rate, tube formation ability, and expression of pathway-related proteins, while ROS content and apoptosis rate were markedly increased (P < 0.05). Compared with the model group, the DZSM blood-absorbed components group showed significantly increased cell viability, migration rate, tube formation ability, and expression of tight junction proteins, as well as significantly decreased ROS content and apoptosis rate (P < 0.05). Moreover, the protein expression levels of HIF-1α and VEGFA were notably upregulated. Molecular docking results indicated strong binding affinities between the blood-absorbed components (e.g., scutellarin) and the HIF-1α/VEGFA targets. In conclusion, the blood-absorbed components of DZSM promote angiogenesis in OGD/R-injured bEND.3 cells, and the mechanism is closely related to activation of the HIF-1α/VEGFA signaling pathway and upregulation of its associated proteins. The experimental protocol strictly adhered to the guidelines of the Ethics Committee of Animal Research of Guangdong Pharmaceutical University (approval No.: gdpulacspf2022137).

This study aimed to investigate the mechanism of the traditional Chinese medicine compound Shengmai Yin (SMY) in exerting anti-myocardial ischemia (MI) effects through the synergistic regulation of the gut microbiota and the MAPK signaling pathway. First, network pharmacology combined with GO and KEGG enrichment analysis was used to predict the potential targets and signaling pathways of SMY against MI. Secondly, an acute myocardial ischemia model was established in SD rats by intraperitoneal injection of pituitrin (25 U·kg^-1), while SMY was administered by intragastric gavage for intervention for 7 days, with daily body weight recording. Subsequently, electrocardiogram and cardiac histopathological changes were detected. The levels of myocardial injury markers [aspartate aminotransferase (AST), creatine kinase (CK), lactate dehydrogenase (LDH), lactic acid (LD), and cardiac troponin-Ⅰ (cTn-Ⅰ)], oxidative stress indicators [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA)] and inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β)] were measured. Immunohistochemistry was used to detect the expression of key apoptosis-related proteins in myocardial tissue, including Bcl-2 associated X protein (Bax), cysteinyl aspartate specific proteinase-3 (Caspase-3), and B-cell lymphoma-2 (Bcl-2). TUNEL staining was used to detect cardiomyocyte apoptosis. Western blot was used to detect the expression levels of key proteins in the mitogen-activated protein kinase (MAPK) signaling pathway. 16S rRNA sequencing was used to analyze the structural changes of the gut microbiota. The experimental animals were approved by the Experimental Animal Management Committee Ethics Committee of Chengdu University of Traditional Chinese Medicine (Approval No.: 2014 DL-023). Network pharmacology analysis identified pivotal targets including TP53, TNF, MAPK1, MAPK3, and CTNNB1, which are predominantly involved in the MAPK and PI3K-AKT signaling pathways. In vivo studies demonstrated that SMY ameliorated electrocardiographic abnormalities and histopathological lesions, reduced serum levels of myocardial injury biomarkers and pro-inflammatory cytokines, suppressed the phosphorylation of the key MAPK protein p38, downregulated the expression of Bax and Caspase-3, and upregulated Bcl-2. Furthermore, 16S rRNA sequencing revealed that SMY modulated gut microbiota diversity and compositional structure. These findings suggest that SMY exerts cardioprotective effects against myocardial ischemia, potentially by suppressing inflammatory responses and cardiomyocyte apoptosis. This therapeutic effect is associated with the modulation of the MAPK signaling pathway and alterations in gut microbiota composition; however, the precise mechanisms and causal relationships warrant further investigation.

Huanglian Jiedu Decoction (HLJDT) is a classic fever-clearing detoxification prescription, with clear clinical evidence to support its anti-tumor activity. However, its effect on melanoma metastasis and its potential molecular mechanism have not been systematically clarified. In this study, network pharmacology is used to predict the potential active components, therapeutic targets and key signaling pathways of HLJDT that may have an anti-melanoma transfer effect. Based on these findings, a mouse melanoma lung metastasis model was established, and in vivo and in vitro experiments were carried out to verify the anti-transfer effect of HLJDT and explore its potential mechanism. The results show that network pharmacology analysis indicates that HLJDT contains multiple potential anti-melanoma active ingredients and may exert a synergistic anti-tumor effect by regulating multiple key signaling pathways, including cancer-related pathways and JAK-STAT pathways. In vivo experiments showed that HLJDT significantly inhibited melanoma lung metastasis, reduced the number of lung metastasis nodules, and enhanced the anti-tumor immune response. In vitro experiments further confirmed that HLJDT significantly inhibits the proliferation and migration of melanoma cells and induces cell apoptosis, which is closely related to the enhancement of ROS generation and mitochondrial membrane potential destruction. Mechanism research shows that HLJDT inhibits the activation of signal transducer and activator of transcription 3 (STAT3) and its phosphorylation, downgrades the expression of PD-L1 and N-cadherin, and upregulates the expression of E-cadherin, thus inhibiting the invasion and metastasis of melanoma cells and improving the immune microenvironment of tumors. Overall, these findings show that HLJDT has potential in inhibiting melanoma metastasis and reshaping the tumor immune microenvironment, providing a systematic experimental basis for its application as an auxiliary treatment of malignant tumors. This experiment was approved by the Experimental Animal Ethics Committee of Shandong University of Traditional Chinese Medicine (approval No.: SDUTCM20220302025).

This study investigated the anti-malignant effects and molecular mechanisms of glabridin (GLA), a licorice-derived flavonoid, in esophageal cancer. The effects of glabridin on the esophageal cancer cell lines KYSE150 and TE1 were evaluated using CCK-8 assays, colony formation assays, wound-healing assays, and flow cytometry. A systematic analysis was further conducted by integrating RNA sequencing, multi-platform pharmacological prediction, protein-protein interaction (PPI) network analysis, Western blot (WB) validation, molecular docking, cellular thermal shift assay (CETSA) and database mining. Glabridin concentration dependently suppressed cell viability, with 48-hour IC₅₀ values of 37.85 and 20.00 μmol·L^-1 in KYSE150 and TE1 cells, respectively. Notably, 5 μmol·L^-1 inhibited colony formation, while 20 μmol·L^-1 induced G0/G1 arrest (59.99% and 56.68% of cells) and reduced 24-hour migration rates to 30% and 25% (P < 0.000 1). Transcriptomics identified 2 104 differentially expressed genes enriched in ferroptosis, autophagy, and cell cycle pathways. Integrated analysis filtered 66 core targets. PPI network topology revealed cyclin A2 (CCNA2), heat shock protein 90 alpha family class A member 1 (HSP90AA1), cyclin-dependent kinase 2 (CDK2), and mechanistic target of rapamycin kinase (MTOR) as hub genes, with CCNA2 and HSP90AA1 synergizing with obesity to affect prognosis in TCGA esophageal cancer cohorts. WB confirmed downregulation of CCNA2, CDK2, cyclin-dependent kinase 1 (CDK1), snail family transcriptional repressor 2 (SNAI2), and phosphorylated protein kinase B (p-AKT), whereas HSP90AA1 protein levels remained unchanged. Molecular docking demonstrated stable binding of glabridin to the CCNA2 active pocket via hydrogen bonding, π-alkyl, and π-anion interactions. CETSA demonstrated that glabridin enhanced CCNA2 thermal stability, and the proteasome inhibitor MG132 blocked glabridin-induced CCNA2 degradation. DepMap and LinkedOmics Database analyses revealed that CCNA2 promotes esophageal cancer cell proliferation and is associated with cell cycle progression. Collectively, glabridin suppresses esophageal cancer cell proliferation and migration, potentially through modulation of the cell cycle and epithelial-mesenchymal transition (EMT) processes, and CCNA2 may represent a promising therapeutic target for esophageal cancer.

This study investigated the effects of different doses of benzo[a]pyrene (BaP) on the expression of fibroblast growth factor 21 (FGF-21), lipid metabolism, and related genes in HepG2 cells, as well as whether these effects are mediated by the aryl hydrocarbon receptor (AhR). HepG2 cells were treated with 15, 30, and 60 μmol·L^-1 BaP for 24 h. The levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in HepG2 cells were measured. The mRNA and protein expression levels of FGF-21, β-oxidation-related genes [peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyltransferase 1α (CPT-1α), and peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α)], and lipid synthesis-related genes [peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), and stearoyl-CoA desaturase 1 (SCD1)] were detected by qPCR and Western blot. A stable cell line with AhR silencing was established via lentiviral transduction, and the cells were treated with 30 μmol·L^-1 BaP. Lipid content was assessed by oil red O staining, and the mRNA and protein expression levels of FGF-21, β-oxidation-related genes, and lipid synthesis-related genes were measured. Compared with the control group, all three doses of BaP (15, 30, and 60 μmol·L^-1) increased the levels of TC, TG, and LDL-C in HepG2 cells. Compared with the 30 μmol·L^-1 BaP group, the 60 μmol·L^-1 BaP group showed higher levels of TC, TG, and LDL-C, lower mRNA and protein expression of FGF-21 and β-oxidation-related genes, and higher mRNA and protein expression of lipid synthesis-related genes. Following AhR silencing and treatment with 30 μmol·L^-1 BaP, lipid content, as well as the levels of TC, TG, and LDL-C, decreased in HepG2 cells, and the mRNA and protein expression levels of FGF-21, β-oxidation-related genes, and lipid synthesis-related genes were all reduced. Different doses of BaP increased lipid content in HepG2 cells. However, low-dose BaP activated AhR, thereby relatively increasing FGF-21 expression, reducing lipid synthesis, and enhancing fatty acid β-oxidation. In contrast, high-dose BaP activated AhR but relatively decreased FGF-21 expression, increased lipid synthesis, and reduced fatty acid β-oxidation. The effects of BaP on FGF-21, lipid metabolism, and related genes are all mediated by AhR.

To explore the mechanism of Mongolian medicine Zixin Dropping Pills (ZXDW) in treating non-alcoholic fatty liver disease (NAFLD), we combined network pharmacology with animal experiments. Network pharmacology identified 59 core targets of ZXDW for NAFLD, and functional enrichment analysis revealed that lipid metabolism pathway and phosphatidylinositol 3-kinase/protein kinase B (PI3K-AKT) signaling pathway were the key involved pathways. Pharmacodynamic experiments on high-fat diet-induced NAFLD in ApoE^-/- mice confirmed that ZXDW alleviated hepatic lipid deposition, fibrosis and inflammation. Immunofluorescence and Western blot verified key targets in the functional pathways, showing that ZXDW significantly upregulated hepatic peroxisome proliferator-activated receptor gamma (PPARγ), liver X receptor alpha (LXRα), ATP-binding cassette subfamily A member 1 (ABCA1) and ATP-binding cassette subfamily G member 1 (ABCG1) protein expression, while downregulating PI3K, AKT and nuclear factor-kappa B (NF-κB) expression in ApoE^-/- mice. Molecular docking between main components of ZXDW and the above targets indicated that costunolide, taurocholic acid and taurodeoxycholic acid might be the main active components. This study preliminarily confirms that ZXDW alleviates NAFLD through lipid metabolism and PI3K-AKT pathways, providing a theoretical basis for its clinical application. The experiment was approved by the Animal Ethics Committee of Inner Mongolia Medical University (approval No. YKD202401262).

Using a molecular hybridization strategy, 17 peptidomimetic derivatives of phenylalanine were designed and synthesized by combining an aminothiazole oxime scaffold with phenylalanine for antibacterial activity studies. The results showed that these compounds exhibited varying degrees of inhibitory activity against the tested bacterial strains, with compound 8p being particularly outstanding. It demonstrated minimal inhibitory concentrations (MIC) of 2 μg·mL^-1 against E. coli, P. aeruginosa, and fluoroquinolone-resistant E. coli (FREC). Its activity against E. coli and P. aeruginosa was comparable to that of the reference drug ciprofloxacin, while its efficacy against FREC was significantly superior to the reference drug. Meanwhile, compound 8p exhibited synergistic effects when combined with certain antibacterial agents. Its relatively significant antibacterial activities and synergistic enhancement warrant further investigation.

The chemical constituents of petroleum ether extracts from the whole plant of Ferula bungeana were isolated using chromatographic techniques such as SiO₂, Sephadex LH-20, and thin-layer chromatography. Their structures were determined through the analysis of their spectral data. Five sesquiterpenoids were identified from the petroleum ether extracts of Ferula bungeana whole plant, namely buntone A (1), caryophyllene oxide (2), eudesol (3), mesoferulone (4), and jaeschkeanadiol (5). Among them, compound 1 was a new sesquiterpene lactone, while compounds 2 and 3 were isolated for the first time from the genus Ferula. Compounds 1-3 were screened for in vitro anti-inflammatory activity, and the results showed that compounds 1-3 exhibited varying degrees of NO inhibitory activity at a concentration of 10 μmol·L^-1, with inhibition rates of 89.8% ± 1.2%, 76.4% ± 0.8% and 80.4% ± 0.9%, respectively.