In the early stages of various diseases—such as COVID-19,influenza,dengue fever,diabetes,pulmonary hypertension and inflammation-driven disorders—failure to intervene promptly can trigger uncontrolled inflammatory responses and multi-system dysfunction,initiating complex pathological cascades that substantially increase morbidity,complication burden,and risk of adverse outcomes.The traditional Chinese medicine(TCM)principle of"preventing disease progression after onset"(Ji Bing Fang Bian)emphasizes early therapeutic intervention to halt disease exacerbation and prevent severe complications.This concept aligns closely with the modern medical strategy of early intervention.This review adopts the TCM theoretical framework of"Ji Bing Fang Bian"to systematically delineate the dynamic progression patterns and key pathophysiological mechanisms underlying the aforementioned conditions.Furthermore,it highlights the unique advantages and clinical value of TCM interventions,which leverage multi-component,multi-target,and multi-pathway synergistic actions to effectively interrupt disease progression.By elucidating the contemporary scientific underpinnings of the"Ji Bing Fang Bian"paradigm,this work aims to provide evidence-informed,and future prospective for the early prevention of these diseases using TCM.
Background: While sulfur fumigation is widely used to preserve Chinese medicinal materials (CMMs), its impact the quality and efficacy of herbal formulas remains unclear. Qiyao Pills (QYP), a proprietary Chinese medicine comprising Astragali Radix, Dioscoreae Rhizoma, Atractylodis Rhizoma, and Scrophulariae Radix, is clinically used for spleen-invigorating and kidney-tonifying effects. Methods: In this study, we investigated the chemical and biological impacts of sulfur fumigation on QYP. First, untargeted and targeted metabolomics were performed to study the chemical variations of QYP formulated with non-fumigated CMMs (NS-QYP) and QYP formulated with sulfur-fumigated CMMs (S-QYP). Second, bioactivity evaluation was conducted to compare the spleen-invigorating and kidney-tonifying effects of NS-QYP and S-QYP. Results: Both untargeted and targeted metabolomics revealed substantial chemical alterations in S-QYP, including degradation of bioactive compounds and formation of sulfur-containing derivatives. Bioactivity evaluation demonstrated that S-QYP exhibited weakened spleen-invigorating and kidney-tonifying effects compared with NS-QYP. Conclusion: These findings provide evidence that sulfur fumigation impacted both chemical quality and pharmacological efficacy of herbal formula, suggesting that those prepared with sulfur-fumigated herbs require careful evaluation before clinical application.
Background: Aconiti radix lateralis praeparata (Fuzi) is widely used for cardiotonic therapy in traditional Chinese medicine, but is limited by toxicity. Licorice-processed aconite (Zhifuzi, ZFZ) is classical processing intended to reduce toxicity while preserving efficacy, yet its comparative effects with HSP and underlying mechanisms in chronic heart failure (CHF) remain unclear. Methods: A rat CHF model was established by abdominal aortic coarctation. After model validation by echocardiography (EF <= 55%), animals received HSP or ZFZ at low, medium and high doses, Shenfu Qiangxin Pills (SFQX) as a positive control, or vehicle for 4 weeks. Cardiac function, plasma biomarkers (BNP, AngII, CK), inflammatory cytokines in cardiac tissue (TNF-alpha, IL-6, IL-10), and histopathology (HE, Masson staining) were assessed. Blood-entry components of ZFZ were profiled by UPLC-Q Exactive-Orbitrap-MS, followed by target prediction, protein-protein interaction analysis, GO/KEGG enrichment and molecular docking. Results: Both ZFZ and HSP improved cardiac function, reduced plasma BNP, Ang II, and CK levels, alleviated inflammatory responses, and attenuated myocardial fibrosis in CHF rats. ZFZ showed relatively better effects than HSP in selected parameters, particularly in the high-dose group. Thirty-one blood-entry metabolites were detected, including 16 prototype compounds. Network pharmacology suggested that alkaloids, flavonoids and triterpenoids target multiple proteins enriched in PI3K-Akt, cAMP and calcium signaling pathways. Docking indicated that talatisamine, oleanolic acid and hetisine exhibited stable binding to MAPK1, PIK3CA and PRKACA, respectively. Conclusion: ZFZ and HSP both exerted cardioprotective effects in CHF rats, while ZFZ showed relatively better effects in selected parameters under the present experimental conditions. The integrated analysis of blood-entry component profiling, network pharmacology, and molecular docking provided preliminary mechanistic clues suggesting that the cardioprotective effects of ZFZ may be associated with multiple components, targets, and pathways. These findings provide comparative pharmacodynamic evidence and a basis for further mechanistic investigation of processed Fuzi in chronic heart failure.
Background: This study aimed to investigate the antitumor efficacy of Pien Tze Huang (PZH) in colorectal cancer (CRC) and elucidate its immunomodulatory mechanism, with a focus on tumor-associated macrophages (TAMs) and colony-stimulating factor 1 receptor (CSF-1R) signaling. Methods: Antitumor effects were evaluated in subcutaneous MC38 allograft and azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CRC mouse models. TAMs infiltration was analyzed via immunohistochemistry and flow cytometry. Macrophage proliferation and migration were assessed by using MTT and Transwell assays. RNA sequencing, RT-qPCR, Western blotting, cycloheximide chase, inhibitor, polysome profiling, and gene silencing assays were performed to determine the mechanism underlying CSF-1R regulation. Results: PZH suppressed mouse CRC growth in both subcutaneous MC38 allograft and AOM/DSS-induced models, with its efficacy being partly dependent on reducing TAMs infiltration. In vitro assays further revealed that PZH impaired macrophage proliferation and migration. Mechanistically, PZH selectively downregulated CSF-1R via a multilayered program involving rapid posttranslational degradation through proteasomal and lysosomal pathways, as well as receptor proteolytic cleavage mediated by the TLR2-iRhom2-ADAM17 axis. Conclusion: Our experiments identify TAMs and CSF-1R as key cellular and molecular targets of PZH, thereby highlighting its ability to modulate TAMs within the tumor microenvironment (TME) and inhibit CRC progression. These results provide mechanistic insights into the immunomodulatory actions of PZH and identify CSF-1R as a promising target for macrophage-targeted therapies in CRC.
Tumor occurrence and development are co-regulated by extracellular matrix(ECM)stiffness and the intratumoral microbiota.This paper first systematically summarizes how matrix stiffness affects the composition and function of the intratumoral microbiota.It then analyzes the regulatory roles of microbiota alterations in tumor occurrence and progression.Furthermore,it summarizes the mechanisms by which bacteria drive tumor progression,including inflammatory activation,metabolic reprogramming,and regulation of oncogenic signaling pathways.On this basis,the anti-tumor mechanisms of Chinese herbal medicines targeting the multi-dimensional regulatory network of the"matrix stiffness-bacteria-tumor"axis are discussed.This review provides an important theoretical basis for understanding bacterium-tumor interactions and for developing Chinese herbal medicine-based therapeutic strategies targeting this axis.
Background:Hepatocellular carcinoma(HCC)is characterized by high malignancy and therapeutic resistance.Salvianolic acid B(Sal B)exhibits antitumor activity,but its underlying molecular mechanisms in HCC remain unclear.Methods:Network pharmacology,quantitative proteomics,molecular docking,biolayer interferometry(BLI),and molecular dynamics simulations were integrated to investigate the anti-HCC mechanism of Sal B.Western blotting and in vivo tumor experiments were further performed.In addition,a liposomal nanoplatform(SalB/ICG@Lip)was developed to improve delivery efficiency.Results:Integrated analysis identified macrophage migration inhibitory factor(MIF)as a potential upstream regulatory target of Sal B.Sal B suppressed the PI3K-AKT-mTOR signaling pathway by reducing MIF expression and decreasing PI3K and AKT phosphorylation.Meanwhile,BLI and computational analyses supported a potential interaction between Sal B and LC3B.Sal B also reduced phosphorylation of mTOR,ULK1,and TFEB while increasing the LC3B-Ⅱ/Ⅰ ratio,suggesting enhanced autophagic activation.Moreover,SalB/ICG@Lip exhibited improved cellular uptake and enhanced antitumor efficacy in vivo with favorable biosafety.Conclusion:Sal B suppresses HCC progression through coordinated regulation of the PI3K-AKT-mTOR axis and autophagy-related pathways.The SalB/ICG@Lip nanoplatform further enhances therapeutic efficacy,supporting the potential of Sal B-based nanotherapeutic strategies for HCC treatment.
Infectious diseases pose a severe threat to global human and animal health,as the escalating spread of antimicrobial resistance increasingly undermines conventional public health systems.Natural Chinese herbal formulations offer a promising alternative due to their favorable safety profiles and broad-spectrum bioactivity in vivo.Pulsatilla decoction(PD),a classical traditional Chinese medicine(TCM)formulation,has been historically employed to"clear heat and detoxify,"specifically targeting febrile diseases and enteric infections.Rooted in the"Sovereign-Minister-Assistant-Messenger"(Jun-Chen-Zuo-Shi)hierarchical principle,PD is precisely composed of four herbs:Pulsatilla chinensis(Bunge)Regel(Sovereign),Coptis chinensis Franch.,Phellodendron chinense Schneid.(Minister),and Fraxini Cortex(Assistant).This structured formulation transcends direct pathogen eradication,functioning instead as a sophisticated host-directed therapy.Its therapeutic efficacy stems from synergistic interactions among alkaloids,saponins,and coumarins,which collectively modulate inflammatory signaling cascades(e.g.,TLR4/NF-κB/MAPK),reinforce intestinal barrier integrity,and restore microbial homeostasis.In this review,we provide a comprehensive synthesis of the chemical constituents,extraction techniques,and multi-level mechanisms of action of PD,with a particular focus on the interplay between its phytochemical profile and host-directed anti-inflammatory and intestinal protective effects.This overview aims to offer critical insights into developing alternative strategies to combat bacterial infections by leveraging the synergistic potential of TCM.However,PD's multi-component nature,unclear precise targets,and variability in extraction methods present challenges for standardization and clinical translation.To advance the application of PD from traditional use to evidence-based applications in both human and veterinary medicine,we have written this review by integrating existing literature.
Background:Acute lung injury(ALI),a critical respiratory condition,represents a significant global health challenge due to its high incidence rates around the world.Qingwen Baidu Decoction(QWBD)is a classical formula with anti-inflammatory effects and antioxidant characteristics.It plays an integral part in infectious disease management.However,the mechanism by which QWBD combats ALI remains markedly unexplored.In order to clarify the preventive efficacy and underlying mechanisms of QWBD in ALI,this study utilized a multi-approach strategy combining network pharmacology,molecular docking,and in vitro/in vivo studies was adopted.Methods:Network pharmacology was utilized to search for bioactive components,key targets and signaling pathways of QWBD against ALI.Molecular docking served as a key method to verify how the principal active monomers in QWBD bind to the identified core targets.Ultra-performance liquid chromatography(UPLC)was used to characterize the chemical compounds of QWBD.Next,we developed both a RAW264.7 cell injury model and a rat model of ALI using LPS.Finally,the effectiveness and mechanism of QWBD in ALI were demonstrated through combination of in vivo/in vitro studies.Results:The network pharmacology results revealed 221 principal bioactive compounds and 217 overlapping core targets between QWBD and ALI.According to GO and KEGG enrichment analyses,QWBD's mechanism of action appears to involve the modulation of genes related to inflammation,apoptosis,and oxidative stress,along with the TLR4-JNK and PI3K-Akt pathways.Among the QWBD compounds,quercetin,kaempferol,β-sitosterol,luteolin,and wogonin were present in high concentrations.Molecular docking analysis confirmed the strong interaction between the five bioactive components and their corresponding targets docking targets.The results of these experiments confirmed that QWBD markedly alleviated ALI via its ability to ameliorate pulmonary edema,inflammatory cell infiltration,as well as cytokine levels while restoring alveolar structural integrity.Conclusion:QWBD exerts its protective effects by modulating the PI3K/Akt and TLR4/JNK signaling pathway.Overall,QWBD protects against LPS-induced ALI,highlighting its potential as a novel preventive agent.
Alopecia is a highly prevalent dermatological disorder characterized by dysregulation of hair follicle cycling,stem cell exhaustion,inflammatory activation,and hormonal imbalance.Currently approved pharmacotherapies provide limited efficacy and are often associated with adverse effects,highlighting an unmet need for multi-targeted and biologically integrative treatment strategies.Traditional Chinese Medicine(TCM),with its long-standing clinical use and multi-component,multi-target characteristics,has emerged as a promising complementary approach for hair loss management.In this review,we integrate hair follicle biology with classical TCM theory to elucidate the mechanistic basis of TCM interventions in alopecia.We summarize key molecules and cellular processes underlying hair loss,including hair follicle stem cell dysfunction,androgen-androgen receptor signaling,oxidative stress-induced aging,immune dysregulation,and impaired angiogenesis.Frequently prescribed TCM herbs and representative formulas,such as Polygonum multiflorum,Platycladus orientalis,Angelica sinensis,and Shi-Bi-Man,are discussed with respect to their bioactive constituents and experimental effects on dermal papilla cells,stem cell activation,inflammatory pathways,and follicular microcirculation.Although some pharmacological and preliminary clinical evidence support the therapeutic potential of TCM for treating alopecia,substantial challenges remain,including insufficient standardization of herbal preparations,limited mechanistic validation,and a lack of high-quality randomized controlled trials.Future integration of systems pharmacology,multi-omics technologies,and advanced drug-delivery platforms may facilitate the translation of TCM from empirical practice to evidence-based therapy for hair loss.
