Thioredoxin-interacting protein in fibrotic diseases: Mechanisms and therapeutic strategies.

Cimifugin relieves the relapse of allergic asthma via inhibiting ILC2 migration by targeting CCR9.

Glioma is a common primary solid brain tumor with high incidence and poor prognosis. Biochanin A (bioA), an active component of traditional Chinese medicine, has potential therapeutic effects on it, but its mechanism remains unclear. This study aimed to clarify its mechanism via a multi-omics strategy. A multi-omics integration approach was adopted, which combined single-cell RNA sequencing, in vitro experiments, the construction of a Glutathione S-transferase P1 (GSTP1)-based prognostic model, and analyses of immune infiltration and drug sensitivity to evaluate its clinical value. C2 CENPF⁺ tumor cells were specifically expressed in recurrent gliomas and associated with the bioA pathway. GSTP1 was the key target gene of bioA; its high expression was related to poor prognosis, and its knockout could inhibit glioma progression. The GSTP1-based prognostic model had excellent predictive efficiency. BioA may exert anti-glioma effects by regulating GSTP1, providing theoretical support for its clinical application and a new therapeutic target for glioma.

Accurate analysis of pharmaceutical and toxic molecules is crucial for public health and safety. Nanozymes, nanomaterials with enzyme-like catalytic activities, have emerged as transformative tools to address this need. This review begins by classifying nanozymes and defining their core properties, followed by a systematic summary of how they integrate with major detection technologies, including colorimetry, fluorescence, electrochemistry, immunoassays, surface-enhanced Raman spectroscopy (SERS), and emerging multimodal techniques to enhance analytical performance. It then presents specific applications across diverse pharmaceutical and toxic targets, such as antibiotics, pesticides, traditional Chinese medicine components, toxins, and drug metabolites. The review further addresses critical challenges, including catalytic efficiency, selectivity, and biocompatibility, and outlines future directions for rational design and intelligent diagnostics. By providing a comprehensive overview of recent advances and persistent hurdles, this review aims to pave the way for continued innovation and practical translation in the field of nanozyme-based detection.

Wilson's disease (WD) is a rare autosomal recessive disorder characterized by impaired copper metabolism and progressive multi-organ damage. Emerging evidence suggests that gut microbiota dysbiosis and reduced microbial fermentation capacity may contribute to the progression of liver diseases. However, whether the gut microbiota can serve as a therapeutic target in WD remains unclear. This study aimed to investigate the modulatory effects of Lycium barbarum polysaccharides (LBPs), a bioactive component of the traditional Chinese medicine Gan-Dou-Fu-Mu decoction, on gut microbiota composition and short-chain fatty acids (SCFAs) production in WD, and to explore their potential as microbiota-targeted prebiotic interventions. WD-associated microbiota exhibited decreased microbial diversity and significantly lower SCFAs production, particularly acetic acid and total SCFAs, compared to healthy controls. LBPs supplementation significantly increased the relative abundances of beneficial genera, including Lactobacillus, Lacticaseibacillus, and Paraeggerthella, as well as SCFAs-producing species such as Bacteroides fragilis and Lactobacillus delbrueckii. Notably, LBPs markedly enhanced acetic acid and total SCFA concentrations in WD microbiota, outperforming the standard treatment agent penicillamine. These findings highlight the promising prebiotic potential of LBPs and support their application as a novel microbiota-targeted adjunctive therapy for WD.

Cancer-related cognitive impairment (CRCI) is a prevalent and clinically significant sequela of cancer and its treatment, markedly reducing quality of life. As a core component of Traditional Chinese Medicine, acupuncture is a potential therapeutic intervention for CRCI; however, conclusive evidence on its efficacy and safety is lacking due to fragmented and methodologically limited studies. This systematic review and meta-analysis aimed to evaluate the efficacy and safety of acupuncture for CRCI. We systematically searched eight databases from inception to February 1, 2025, for randomized controlled trials (RCTs) in adults with CRCI comparing acupuncture with control interventions (e.g., conventional care, sham acupuncture, and other active therapies). Risk of bias was assessed using the Cochrane tool (v1). Meta-analyses used RevMan 5.3. Evidence certainty was evaluated with the GRADE framework. Prespecified subgroup analyses explored heterogeneity by acupuncture modality, treatment duration, cancer treatment phase, and cancer type. Forty-four RCTs (n = 3,783) were included. Versus conventional treatment, acupuncture significantly improved Mini-Mental State Examination (MMSE) scores (mean difference [MD] = 2.34, 95% confidence interval [CI] [1.84, 2.85], P < 0.00001), Montreal Cognitive Assessment (MoCA) scores (MD = 1.48, 95% CI: [1.15, 1.82], P < 0.00001), and reduced postoperative cognitive dysfunction (POCD) incidence (risk ratio [RR] = 0.49, 95% CI: [0.41, 0.60], P < 0.00001). Compared with sham acupuncture, acupuncture improved MMSE (MD = 2.48, 95% CI: [1.55, 3.41], P < 0.00001) and MoCA (MD = 1.52, 95% CI: [0.16, 2.88], P = 0.03) scores, though the latter was imprecise. Acupuncture demonstrated no significant benefit for the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 cognitive subscale compared with sham acupuncture (P = 0.11) or other active therapies (P = 0.15). Subgroup analyses identified treatment duration, acupuncture modality, and cancer type as major heterogeneity sources. Safety reporting was often incomplete, yet all documented adverse events were mild and transient. Grading of Recommendations Assessment, Development and Evaluation evidence certainty was low to very low. Acupuncture may improve global cognitive function and reduce POCD incidence in CRCI. However, the safety profile requires further confirmation. Current evidence is limited by methodological weaknesses, substantial heterogeneity, and imprecision, highlighting the need for rigorous, high-quality RCTs with standardized protocols, objective biomarkers, and comprehensive safety monitoring to define acupuncture's role in CRCI management.

Constructing rosin-based quaternary ammonium salt-functionalized silica stationary phase for versatile chromatographic separations.

Hyperlipidemia, a common metabolic disorder marked by elevated serum lipids like total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C), raises risks for cardiovascular diseases, atherosclerosis, nonalcoholic fatty liver disease, and diabetes. Conventional treatments like statins have limitations, including liver damage and resistance, driving interest in natural compounds with multi-target, low-toxicity effects. This study assessed Astragalus polysaccharide (APS), a traditional Chinese medicine component with antioxidant and metabolic-regulatory properties, for its therapeutic effects on hyperlipidemic rats and its mechanism via the miR-128-3p/NRF2/antioxidant pathway. SD rats were grouped into normal, model, simvastatin, and APS. Except normal, all received high-fat diet for 8 weeks to induce hyperlipidemia. Then, APS (700mg/kg) or simvastatin (6.7mg/kg) was administered via gavage for 8 weeks; controls received saline. Serum indices were monitored periodically; pancreatic and hepatic tissues were analyzed histologically and molecularly. In vitro, lipid accumulation was induced in BRL and HepG2 cells with oleic/palmitic acids (2:1). Optimal APS dose/time was determined by CCK-8; lipid and oxidative markers were measured. A high-fat diet caused hyperlipidemia, elevating lipids, body weight, and energy intake. APS reduced glucose/lipid levels, and transaminase activity and improved pancreatic/hepatic pathology, including β-cell function. APS lowered MDA and miR-128-3p while boosting T-SOD and hepatic NRF2. In cells, APS reversed lipid buildup and oxidative stress. APS mitigates hyperlipidemia via the miR-128-3p/NRF2/antioxidant pathway, providing a multi-target strategy for lipid metabolism, oxidative stress, and organ protection. This supports natural interventions for hyperlipidemia, especially with glucose/organ issues, meriting clinical exploration.

Metanephric mesenchymal cells (MMCs) hold therapeutic potential for acute kidney injury (AKI), but their efficacy is limited, and the mechanisms underlying their action remain unclear. This study aimed to investigate whether catalpol-pretreated MMCs (MMCs-cata) could enhance the efficacy of AKI treatment by regulating key signaling pathways. An AKI model was established in C57BL6 mice via intraperitoneal injection of cisplatin, and the therapeutic effects of MMCs-cata were compared with those of untreated MMCs. RNA-Seq was performed to analyze differentially expressed genes, Western blotting and ELISA were used to measure VEGF-A levels in MMC-cata and the supernatants. An in vitro model of cisplatin-induced renal tubular epithelial cell injury was developed to investigate the signaling pathways upstream and downstream of VEGF-A. The role of VEGF-A/VEGFR2 was confirmed through experiments involving gene silencing, neutralizing antibodies, and VEGFR2 blockade. Additionally, molecular docking simulations and Western blotting were performed to explore the effects of catalpol on the Wnt signaling pathway. MMCs-cata significantly improved renal function in AKI model mice by suppressing inflammation, oxidative stress, and necroptosis. RNA-Seq, Western blotting and ELISA revealed the activation of VEGF-related genes in MMCs-cata along with elevated intracellular and supernatant VEGF-A levels. In both the in vivo and in vitro models, silencing VEGF-A in MMCs-cata, neutralizing VEGF-A in the supernatant, or blocking VEGFR2 in tubular epithelial cells abolished the protective effects of MMCs-cata, while exogenous VEGF-A supplementation alone exerted protective effects. Mechanistic studies indicated that MMCs-cata activated the p38 pathway and suppressed the STAT3 pathway. Molecular docking and Western blotting confirmed that catalpol binds to Wnt3A, activating the canonical Wnt pathway to drive VEGF-A secretion. Catalpol pretreatment enhances the therapeutic efficacy of MMCs by activating the canonical Wnt pathway to promote VEGF-A secretion. VEGF-A interacts with VEGFR2 on renal tubular epithelial cells, likely through both p38 pathway activation and STAT3 pathway inhibition, thereby suppressing inflammation, oxidative stress, and necroptosis to alleviate AKI. This study provides novel insights into the integration of traditional Chinese medicine components with stem cell therapy for AKI management.

Background: Co-delivery of two drugs with diverse physicochemical properties and a specific administration sequence holds great importance in cancer theranostics to overcome drug resistance and reduce side effects. Paclitaxel (PTX) and hydroxycamptothecin (HCPT) have long been used clinically as chemotherapeutic agents for Nasopharyn-geal carcinoma (NPC). However, their clinical application is severely restricted by low water solubility, poor stability, and systemic adverse reactions. Nanoparticle-based drug delivery systems provide a promising platform for combination cancer therapy. Methods: In this study, folic acid-modified and dual drug-loaded self-assembled HCPT/PTX@FA@p-PS-SPIONs were successfully fabricated via the emulsification–solvent evaporation method using amphiphilic phosphorylated polystyrene (p-PS). The characterization, cellular uptake, and in vivo pharmacokinetic profiles of the nanoparticles in NPC models were systematically investigated. Result: HCPT/PTX@FA@p-PS-SPIONs were successfully prepared with p-PS as the copolymer backbone. The nanoparticles exhibited a uniform particle size of 196.9 ± 5.5 nm and a zeta potential of −7.3 ± 0.7 mV. The encapsulation efficiency (EE) was 81.4 ± 2.5% for PTX and 67.6 ± 4.1% for HCPT. The drug loading (DL) efficiency was 18.4 ± 1.5% for PTX and 12.2 ± 1.0% for HCPT. HCPT/PTX@FA@p-PS-SPIONs showed favorable biocompatibility. Sustained and sequential release of the two drugs contributed to an enhanced therapeutic effect. Moreover, under magnetic field (MF) guidance, HCPT/PTX@FA@p-PS-SPIONs exhibited stronger inhibitory effects on NPC cells than single-drug, cocktail, or dual-drug groups, demonstrating the superiority of the combined therapy. Pharmacokinetic studies in rats revealed that the half-lives of PTX and HCPT were 3.9 ± 1.2 h and 4.7 ± 1.1 h, respectively, confirming that HCPT/PTX@FA@p-PS-SPIONs could resist rapid metabolism and clearance in vivo. Conclusions: The long-circulating, folic acid-targeted nanoparticles HCPT/PTX@FA@p-PS-SPIONs show great potential for the targeted therapy of nasopharyngeal carcinoma.

BackgroundGlycemic variability is increasingly recognized as an important contributor to the development of diabetes-related complications in patients with type 2 diabetes mellitus (T2DM). Continuous subcutaneous insulin infusion (CSII) is effective in improving glycemic control; however, fluctuations in blood glucose can persist. Mulberry twig alkaloids (MTA), a traditional Chinese medicine component with hypoglycemic properties, have shown potential benefits in regulating glucose metabolism. This study aimed to evaluate whether MTA combined with CSII could further improve glycemic variability and symptoms recognized by traditional Chinese medicine (TCM) in patients with T2DM.Material/MethodsSixty hospitalized patients with T2DM were randomly assigned to a control group (CSII alone, n=30) or an MTA group (MTA tablets plus CSII, n=30). Flash glucose monitoring was used to assess glycemic variability indicators, including mean blood glucose (MBG), standard deviation of blood glucose (SDBG), coefficient of variation (CV), mean amplitude of glycemic excursions (MAGE), mean of daily differences (MODD), time in range (TIR, 3.9–10 mmol/L), time above range (TAR), and time below range (TBR) over 14 days. TCM symptom scores were evaluated before and after treatment.ResultsAfter 14 days, MODD, MAGE, TAR, and TBR were significantly lower in the MTA group compared with the control group (all P<0.05), while TIR was significantly higher (P<0.01). Additionally, the TCM symptom score was markedly reduced in the MTA group compared with the control group (P<0.05).ConclusionsOur findings suggested that CSII combined with mulberry twig alkaloids can improve blood glucose variability and relive TCM symptoms in T2DM patients.Chinese Clinical Trail Registry (NO. ChiCTR 2200062688)

Breast cancer (BC) is a leading global malignancy in women. Although central to treatment, chemotherapy may paradoxically promote metastasis. The role of metabolic changes in chemotherapy- induced metastasis remains unclear. This study aims to investigate the association between metabolic alterations and BC metastasis after CMF (cyclophosphamide (CCP), methotrexate (MTX), and 5-fluorouracil (5-FU)) chemotherapy. A murine BC model treated with CMF was used. Metabolomic profiling identified altered pathways. Metastasis was assessed via tumor growth, hematoxylin and eosin (H&E), and immunohistochemistry (IHC). Phospholipid metabolism was inhibited with idelalisib combined with CMF. Traditional Chinese medicine (TCM) components were screened. Epicatechin (EC) was identified as a modulator of phospholipid metabolism and tested in CMF. Metabolomic analysis revealed a marked upregulation of phospholipid metabolism in CMF-treated BC mice, which was linked to enhanced metastasis. Intervening with idelalisib in combination with CMF abolished these protumorigenic effects. Among the screened TCM components, EC was identified as a modulator of phospholipid metabolism. Similarly, the combination of EC and CMF maintained chemotherapy's antitumor efficacy while substantially reducing metastatic spread. Our findings reveal that CMF chemotherapy induces phospholipid metabolic reprogramming, which drives BC metastasis. Targeting this pathway-either through pharmacological inhibitors (idelalisib) or natural compounds (EC)-can mitigate chemotherapy-induced metastasis without compromising tumor suppression. This suggests that metabolic modulation could be a viable strategy to enhance chemotherapy efficacy. Upregulated phospholipid metabolism is a critical mechanism behind chemotherapy-induced BC metastasis. Combining CMF with phospholipid-targeting agents (idelalisib or EC) offers a promising therapeutic approach to optimize chemotherapy outcomes. These results provide a theoretical foundation for developing novel combination therapies in BC treatment.

Auricularia auricula polysaccharide attenuates Rhizoma Dioscorea bulbifera decoction-induced hepatotoxicity by regulating the TNF-α/PI3K/AKT pathway and gut microbiota.

Based on the theory of ″Qu-Zhi-Bu-Yi″, this study aimed to investigate the optimal compatibility ratio of Angelicae Pubescentis Radix and Taxilli Herba for preventing and treating pressure-induced human nucleus pulposus(NP) cell apoptosis, and to elucidate the mechanisms. A human NP cell apoptosis model was established using abnormal mechanical pressure at 1.0 MPa. The concentration ratios of quercetin, osthole, and columbianadin were screened by the orthogonal experimental design. Cell proliferation and apoptosis were determined using the cell counting kit-8(CCK-8) assay and Annexin V-APC/PI double staining, respectively. Western blot was performed to detect apoptosis-related proteins, as well as key protein expressions in the phosphatase and tensin homolog(PTEN)-induced putative kinase 1(PINK1)/Parkin-mediated mitophagy pathway, and the nuclear factor erythroid 2-related factor 2(Nrf2)-mediated antioxidant pathway. Mitochondrial ultrastructure was observed by transmission electron microscopy(TEM). Mitochondrial membrane potential was measured using the JC-1 staining. Oxidative stress markers were evaluated by the enzyme-linked immunosorbent assay(ELISA). Energy metabolism was quantified using colorimetry. Reactive oxygen species(ROS) levels were detected using the 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA) fluorescent probe. The Nrf2 overexpression and knockdown model construction efficacy in NP cells was validated by quantitative real-time polymerase chain reaction(qRT-PCR). Additionally, rescue experiments were designed to validate the mechanism of the above pathways. Based on the results, the optimal combination of quercetin at 50 μmol·L~(-1), osthole at 6.25 μmol·L~(-1), and columbianadin at 12.5 μmol·L~(-1) significantly promoted NP cell proliferation and inhibited apoptosis. The components enhanced mitophagy by activating the PINK1/Parkin pathway and alleviated oxidative stress by activating the Nrf2 pathway. Rescue experiments showed that the anti-apoptotic effects of the traditional Chinese medicine(TCM) components could be reversed by mitophagy inhibition and Nrf2 knockdown. In conclusion, the Angelicae Pubescentis Radix-Taxilli Herba components inhibit pressure-induced NP cell apoptosis by synergistically activating PINK1/Parkin-mediated mitophagy and Nrf2-mediated antioxidant response. These findings provide experimental evidence for intervertebral disc degeneration treatment.

Enhanced bioavailability of anemoside B4 by dry powder inhalation mitigates high-altitude acute lung injury.

Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease. Current treatment options have limitations in terms of efficacy and side effects. TAS2R38 is an important bitter taste receptor, and recent studies have suggested its potential role in gut immune regulation. This study aims to explore the role of the TAS2R38 receptor in UC and evaluate its potential as a therapeutic target. A 3% DSS solution was used to induce colitis in mice. The expression of TAS2R38 and its downstream signaling pathway was assessed using immunohistochemistry, Western blot, and immunofluorescence. Through molecular docking and pharmacological screening, bitter compounds, that bind to TAS2R38 were identified. The therapeutic effects of bitter compounds on DSS-induced colitis were evaluated by monitoring body weight, measuring colon length, conducting HE staining, and assessing the mucus layer integrity. In the DSS-induced colitis mouse model, the TAS2R38 signaling pathway was found to be inhibited, particularly with a significant reduction in the expression of the downstream proteins PLCβ2 and IP3R3. Pharmacological screening and molecular dynamics simulations revealed that berberine strongly binds to TAS2R38 and effectively prevents DSS-induced colitis by activating this receptor. Berberine treatment significantly alleviated symptoms such as weight loss, diarrhea, and fecal occult blood, and improved colon length, spleen weight, and disease activity index (DAI). Additionally, HE staining showed that berberine significantly reduced DSS-induced epithelial damage and restored intestinal mucus barrier integrity. This study suggests that the TAS2R38 receptor may play a key role in the pathogenesis of ulcerative colitis. Berberine, by activating the TAS2R38 signaling pathway, exerts significant protective effects in DSS-induced colitis. TAS2R38 could be a potential therapeutic target for UC, and berberine, as a traditional Chinese medicine component, holds promise as a treatment for UC.

Migraine is a common chronic episodic brain dysfunction disorder with high prevalence and disability rates worldwide. It severely impacts patients’ quality of life and imposes a heavy socioeconomic burden. Neurogenic inflammation plays a pivotal role in migraine pathogenesis, with tumor necrosis factor-α (TNF-α) serving as a key inflammatory mediator involved in the disease process. Traditional Chinese Medicine (TCM) offers unique insights into migraine pathogenesis through concepts like meridians and qi-blood dynamics. Additionally, certain active components in Chinese herbal medicines demonstrate effects on TNF-α and migraine. Future drug development targeting TNF-α and integrated treatment strategies hold promise for breakthroughs in migraine management. Research combining TCM and Western medicine will further expand therapeutic possibilities, thereby improving treatment outcomes and quality of life for migraine sufferers.

This study introduces the practice of Chemistry of Chinese Materia Medica teaching, aiming to both strengthen the integration of theory and practice and enhance students’ professional competencies through the application of AI technology. Guided by the core competency requirements for relevant professions, we have restructured the content of the course, introduced innovative teaching models, and optimized the evaluation methods. These reforms specifically include virtual simulation, knowledge graphs, and intelligent evaluation. The implementation of these practices will enhance core competencies of undergraduates in traditional Chinese medicine component analysis, quality control, and research, aligning university education with industry demands and providing a reference for the cultivation of traditional Chinese medicine professionals.

Liver fibrosis results from an imbalance between the deposition and the degradation of the extracellular matrix in the liver, for which there are currently no effective therapeutic drugs available. In this study, we demonstrated that baicalin, a major active component of the traditional Chinese medicine Scutellaria baicalensis, was able to inhibit the activation of hepatic stellate cells and attenuate liver fibrosis in various mouse models. In order to elucidate the molecular basis of its antifibrotic effects, we designed a novel baicalin photo-cross-linking probe and applied a quantitative chemoproteomic strategy based on dimethyl labeling to profile baicalin-interacting proteins. Aided by systematic gene knockouts of these potential baicalin interactors, we identified STAT3 as a key target in mediating the antifibrotic function of baicalin. Mechanistically, baicalin primarily binds to the N-terminal domain of STAT3, inhibits its interaction with JAK2 and thereby suppresses STAT3 phosphorylation. Our findings reveal the molecular mechanism of the antifibrotic effects of baicalin and provide a theoretical basis for the design of new antifibrotic drugs based on the structure of baicalin.

The Hippo signaling pathway, as a highly conserved tumor suppressor pathway, is closely related to the occurrence and development of various malignant tumors due to the abnormal expression of its core components, mammalian STE20-like protein kinase 1/2(MST1/2), large tumor suppressor kinase 1/2(LATS1/2), and effector factor Yes-associated protein 1(YAP)/WW domain-containing transcription regulator 1(TAZ). This pathway plays a key regulatory role in pathological processes such as malignant proliferation, apoptosis, and drug resistance by regulating downstream target genes such as connective tissue growth factor(CTGF) and cysteine-rich angiogenic inducer 61(CYR61). Currently, it has been found through research that effective components of traditional Chinese medicine(TCM) and TCM formulas can exert anti-cancer effects by regulating the Hippo signaling pathway, but the specific targets and biochemical processes involved remain unknown. This article integrated the action targets and regulated biochemical processes of effective components of TCM targeting the Hippo signaling pathway in anti-tumor activities and discovered that flavonoids, terpenoids, glycosides, and other effective components of TCM and TCM formulas can regulate the Hippo signaling network, with the most significant mechanisms being the intervention of YAP/TAZ nuclear-cytoplasmic shuttling, restoration of the activity of Hippo core kinases, and blocking of crosstalk between pathways. Taking the Hippo pathway as the research object not only provides a new perspective for explaining the scientific connotation of TCM in anti-tumor activities but also lays a theoretical foundation for the development of new TCM drugs based on Hippo pathway-targeted therapy.