Chinese Medicine最新文献

Background: A pathological link exists between mitochondrial fission/fusion imbalance and cardiovascular disease (CVD). Traditional Chinese Medicine (TCM), based on concepts such as "Qi stagnation and blood stasis" and "Yin-Yang imbalance," helps balance mitochondrial function through the combined effects of multiple components, providing a comprehensive treatment approach for CVD.

Aims of the study: To methodically clarify the molecular processes by which TCM formulations, extracts, and bioactive compounds target mitochondrial dynamics to intervene in CVD over the past five years, highlighting their ethnopharmacological significance in "multi-component and multi-target" synergistic actions.

Methods: This study searched PubMed, Web of Science, Wanfang, and VIP databases (2019-2024), using the Boolean search formula: ("cardiovascular disease" OR "CVD") AND ("mitochondrial dynamics" OR "mitochondrial fission" OR "mitochondrial fusion") AND ("Traditional Chinese Medicine" OR "TCM") AND ("active compounds" OR "bioactive components"). After deduplication with EndNote, 183 articles were systematically screened and included, comprising in vitro experiments using cardiomyocyte models, in vivo studies based on animal models of CVD, and mechanistic investigations utilizing ex vivo tissues or cellular experiments (all human clinical trials were excluded).

Results: Formulations such as Buyang Huanwu Decoction (BYHWD) and Qishen Yiqi Dropping Pills (QSYQ) improved heart conditions by reducing dynamin-related protein 1 (Drp1) overactivity and increasing mitofusin 2 (Mfn2) and optic atrophy 1 (OPA1) levels. Bioactive compounds, such as salidroside(Sal), prevented Drp1 from causing mitochondria to split apart by activating the AMP-activated protein kinase(AMPK)/Sirtuin 1(SIRT1) pathway, while astragaloside IV facilitated better mitochondrial fusion to enhance energy utilization.

Conclusion: TCM manages mitochondria dynamics through multi-target mechanisms, connecting "overall treatment" with "specific targeting" for heart disease therapy. Further ethnopharmacological translation requires standardized screening of bioactive components and the development of innovative drug delivery systems. The study suggests a "Traditional Chinese Medicine-Mitochondrial Dynamics Intervention Model (TCM-MDIM)," which combines organelle-level mitochondrial regulation with the principle of balancing blood and qi to offer novel approaches to the targeted therapy of cardiovascular disorders.

Background: Acute lung injury (ALI) is a severe respiratory inflammatory disorder with high morbidity and mortality. Huangqin Qingfei Decoction (HQQFD), a classic traditional Chinese medicine formulation composed of Scutellaria baicalensis Georgi (Scutellariae Radix, SR) and Gardenica jasminoides Ellis (Gardeniae Fructus, GF), is clinically used for treating respiratory inflammation including ALI. However, the pharmacodynamic basis of HQQFD and the optimal combination of raw and processed forms of SR and GF remain unclear.

Purpose of the research: This study aimed to evaluate the therapeutic differences among four clinical variants of HQQFD and identify key bioactive components using a lipopolysaccharide (LPS)-induced ALI rat model.

Methods: ALI rats were induced by LPS and treated with four HQQFD combinations (different raw/processed forms of SR and GF) at low or high doses. Therapeutic effects were assessed by lung histopathological observation, injury scoring, determination of inflammatory cytokine levels, lung wet/dry (W/D) ratio, and bronchoalveolar lavage fluid (BALF) analysis. Ultra-high performance liquid chromatography-Orbitrap high-resolution mass spectrometry (UHPLC-Orbitrap HRMS) was used to characterize the chemical profiles of different HQQFD variants. Pearson correlation analysis, gray relational analysis (GRA), and Orthogonal partial least squares (OPLS) spectrum-effect relationship analyses were performed to identify efficacy-oriented components.

Results: A total of 113 compounds were identified in HQQFD, among which 49 showed significant differences between raw and processed combinations. High-dose HQQFD groups exhibited superior therapeutic effects compared to low-dose groups, with the combination of wine Scutellariae Radix (WSR) and Gardeniae Fructus Praeparatus (GFP) being the most effective variant. This optimal combination significantly alleviated lung tissue damage, reduced inflammatory cytokine levels, improved lung W/D ratio, and attenuated BALF abnormalities in ALI rats. Spectrum-effect relationship analysis revealed 20 key bioactive components correlated with pharmacodynamic effects, in which 8 compounds include: geniposidic acid, genipin 1-gentiobioside, geniposide, baicalin, glychionide A, wogonoside, oroxylin A and crocetin was detected in lung tissues, these components are more closely related and may synergise more targets in the treatment of ALI.

Conclusion: These findings demonstrate that HQQFD ameliorates LPS-induced ALI in rats by regulating the inflammatory response. The combination of WSR and GFP at high dose shows the best therapeutic effect, and the 20 identified compounds are potential pharmacodynamic substances of HQQFD. This study provides experimental evidence for the clinical optimization and quality control of HQQFD in the treatment of ALI.

Background: The management of dysbiotic gut microbiota in Clostridioides difficile infection has attracted increasing scholarly attention. The development of therapeutic agents with low toxicity, derived from both the flavonoid xanthohumol and the short-chain fatty acid-producing probiotic Clostridium butyricum, holds considerable promise for combating Clostridioides difficile infection. Despite their therapeutic potential, the molecular mechanisms underlying the anti-Clostridioides difficile effects remain inadequately characterized.

Methods: In this study, we established a dextran sulfate sodium-induced inflammatory model using Caco-2 intestinal epithelial cells. The protective effects of xanthohumol against Clostridioides difficile infection superimposed on colitis were evaluated through cell viability assays, analysis of inflammatory signaling pathways, and proteomic profiling. Subsequent in vitro assays and proteomic analyses were conducted to assess the influence of xanthohumol and Clostridium butyricum supernatant on Clostridioides difficile. Furthermore, tandem mass tag-based post-translational modification proteomics was employed to elucidate the underlying molecular mechanisms and key pathways. Finally, critical metabolic enzyme activity assays were performed to validate the regulatory roles of these pathways.

Results: Xanthohumol significantly alleviated C. difficile-induced damage in Caco-2 cells, enhanced cell viability, and suppressed the activation of inflammatory signaling pathways. In vitro experiments demonstrated that both xanthohumol and C. butyricum supernatant reduced bacterial colonization, inhibited growth, and attenuated toxin production. Proteomic analyses revealed substantial alterations in the proteome of C. difficile in response to each treatment. Post-translational modification proteomics further indicated that both treatments modulate lysine acetylation levels, influencing glycolysis pathways and ultimately diminishing the pathogen's virulence. Furthermore, mass spectrometry identified a specific lysine acetylation at the K280 site of fructose-1,6-bisphosphate aldolase, a key enzyme in glycolysis. Functional validation via site-directed mutagenesis confirmed the essential role of this acetylation in regulating the catalytic activity of fructose-1,6-bisphosphate aldolase.

Conclusions: Our study demonstrates that xanthohumol and Clostridium butyricum attenuate the pathogenicity of Clostridioides difficile through modulation of lysine acetylation and disruption of glycolysis metabolism. These findings highlight their potential as promising therapeutic strategies for treating Clostridioides difficile infection.

Despite being widely used to treat cardiovascular disease (CVD), there are still limitations of Traditional Chinese Medicine (TCM) for their widespread use due to undetermined pharmacological mechanisms. The emerging area of "pharmacomicrobiology" facilitates the pursuing of the complex interactions between TCM and gut microbiome as the gut microbiota influences TCM bioavailability and efficacy, vice versa TCM affects the microbial composition and function. Furthermore, research over the past decades has proved that gut dysbiosis and diverse microbial metabolites intimately related to the onset and progression of CVD. Herein, we summarize latest understanding of the TCM-gut-heart axis in CVD, with an emphasis on describing microbial changes and the associated mechanisms in CVD, elaborating the role of gut microbiota in metabolizing TCM, and how TCM can be used to treat CVD through affecting the gut microbiota. We further highlight the challenges and future directions that target TCM-gut-heart axis in prospects for personalized medicine in CVD, thus to present novel insights for developing new therapeutic approaches.

Background: Aberrant microglial activation and impaired adult hippocampal neurogenesis play critical roles in the pathogenesis of depression. Although electroacupuncture (EA) has demonstrated clinical antidepressant efficacy, the underlying mechanisms by which it modulates microglial activity and promotes neurogenesis remain unclear.

Methods: Male C57BL/6 J mice were subjected to chronic unpredictable mild stress (CUMS) for three weeks. Following this period, the mice were divided into groups receiving either EA at the Yintang (GV29) and Baihui (GV20) acupoints, imipramine (IMI) as a positive control, or no treatment (vehicle control) for an additional 3 weeks. To evaluate depressive-like behaviors, we conducted the sucrose preference test, forced swimming test, and tail suspension test. Anxiety-like behaviors were assessed using the open field test and elevated plus maze. We employed immunofluorescence, Golgi staining, Western blotting, and real-time quantitative PCR (qRT-PCR) to elucidate the effects of EA on microglia-driven hippocampal neurogenesis and BDNF signaling. Notably, loss-of-function experiments utilizing PLX5622 for microglial ablation and ANA-12 for TrkB blockade demonstrated the necessity of both microglia and BDNF signaling for the therapeutic efficacy of EA.

Results: EA treatment significantly alleviated CUMS-induced anxiodepressive behaviors. This behavioral recovery was associated with a phenotypic shift in microglia towards a pro-neurogenic state in the hippocampus. Importantly, microglia were essential for the therapeutic effects of EA, as evidenced by their ablation with PLX5622. Furthermore, EA enhanced neurogenesis by orchestrating a multi-step augmentation of BDNF signaling, which involved PKA activation, subsequent release from MeCP2-mediated transcriptional repression, and ultimately increased maturation of BDNF.

Conclusions: Our findings demonstrate that EA exerts antidepressant effects by promoting a pro-neurogenic transformation of microglia. Mechanistically, these microglia enhance BDNF function via the PKA/MeCP2/BDNF pathway, thereby facilitating hippocampal neurogenesis and restoring synaptic plasticity, which collectively alleviate depressive symptoms.

Ethnopharmacological relevance: Hair greying is a common aspect of the natural ageing process. Although it is generally not considered a medical problem, its high prevalence can substantially impact emotional state due to aesthetic concerns. A growing body of research has demonstrated that natural products and their derivatives derived from plants possess advantages and potential in the treatment of hair greying.

Aim of the study: To review the last research progress in the treatment of hair greying by natural products and their derivatives, focusing on the target and mechanism of action of natural products and their derivatives and providing a reference for future clinical use.

Materials and methods: We searched electronic databases (PubMed, Web of Science, ClinicalTrials.gov, and CNKI) for studies published between January 2005 and June 2025. The research focused on the pathogenesis of hair greying and the use of natural products and their derivatives to prevent and treat it, using the keywords: "hair greying", "hair pigmentation", "white hair", "snow hair", "melanocyte stem cells" and "melanin".

Results: Account of natural products (e.g., Polygoni multiflori radix) and their derivatives (e.g., Epimedin B), are expected to treat hair greying due to their various qualities to regulate melanocyte stem cells, enhance melanin synthesis, or promote melanosome transport. Compared to oral administration, topical application represents a preferred approach for promoting hair pigmentation.

Conclusions: We discussed and summarized the mechanism of natural products and derivatives in the treatment of hair greying, which provided a reference for future clinical use.

Rationale: Chronic migraine is characterized by persistent trigeminal sensitization and neuroinflammation. however, the molecular mechanisms underlying its maintenance and mediate the therapeutic effects of acupuncture remian incompletely understood.

Method: A chronic migraine-like state was induced in mice by repeated dural inflammatory soup (IS), followed by electroacupuncture (EA). Behavioral hypersensitivity was assessed, and molecular changes in the spinal trigeminal nucleus caudalis (Sp5C) were analyzed using transcriptomic, biochemical, and functional approaches.

Result: Repeated inflammatory stimulation markedly increased CXCL13 and CXCR5 expression and ERK phosphorylation in the Sp5C, accompanied by mechanical allodynia, thermal hyperalgesia, glial activation, and elevated IL-6 and CCL2 levels. EA significantly attenuated pain hypersensitivity and reduced CXCL13/CXCR5 expression, ERK activation, glial reactivity, and inflammatory mediator release. EA also decreased migraine-related neuropeptides and synaptic plasticity markers, including substance P, PACAP, and NR2B. Functional manipulation experiments demonstrated bidirectional regulation of pain behaviors by CXCR5, establishing its causal role in chronic migraine-like sensitization. MicroRNA profiling identified a dysregulated miRNA signature converging on the transcription factor FOXO3, which indirectly regulated CXCR5 transcription, defining a miRNA-FOXO3-CXCR5 regulatory pathway.

Conclusion: Our study reveals the CXCL13/CXCR5/ERK axis as a previously unrecognized pathway in migraine neuroinflammation and demonstrates electroacupuncture's multimodal therapeutic mechanisms. These findings provide: (1) novel mechanistic insights into migraine pathophysiology through CXCR5-mediated signaling, and (2) translational implications for chronic migraine treatment by targeting the CXCL13/CXCR5/ERK axis. This work establishes a foundation for future development of targeted therapies and validates electroacupuncture as a viable intervention for migraine management.

Background: Psoralea corylifolia(PF) is widely utilized for the treatment of conditions such as kidney yang deficiency, frequent urination, and cold pain in the waist and knees. However, both basic research and clinical reports indicate that it induce hepatotoxicity. Our preliminary research has confirmed that PF has hepatotoxicity and in vitro research indicated that psoralidin is hepatotoxic. but it remains unclear whether psoralidin is the hepatotoxic component of PF and the mechanism of psoralidin induces hepatotoxicity. This study aimed to investigate the hepatotoxicity induced by psoralidin and its toxic mechanisms.

Methods: Kunming mice were used to conduct long-term toxicity experiments. Liver function indices, organ coefficients, and histopathological observations were employed to assess the hepatotoxicity of psoralidin. Non-targeted metabolomics and proteomics analyses were conducted to elucidate the potential pathways and targets associated with psoralidin-induced hepatotoxicity. Furthermore, immunofluorescence staining, molecular docking and Western blotting analyses were utilized to validate the mechanisms underlying psoralidin hepatotoxicity.

Results: The elevation of ALT and AST, accompanied by hepatic steatosis and lipid droplet aggregation were observed after psoralidin treatement. Psoralidin affected biosynthesis of unsaturated fatty acid, fatty acid metabolism, arachidonic acid metabolism, phospholipid metabolism, and oxidative phosphorylation. Further validation research found that psoralidin induced the expressions of Acot4 and Plin5, which in turn caused up-regulations of TGs and FFA in mice, and increased the HSD17B12 level, thereby promoting the synthesis of long-chain fatty acids and facilitating lipid synthesis. And psoralidin catalyzed the conversion of phosphatidylcholine into LPC by enhancing Pla2g6 and Pla2g12b levels, which promoted the synthesis and accumulation of TGs, ultimately inducing disorders in glycerophospholipid metabolism. Furthermore, psoralidin caused upregulation of ROS and mitochondrial damage, leading to a decrease in FA oxidation.

Conclusion: Psoralidin is one of the hepatotoxic components of PF, which induced hepatotoxicity via promoting lipid synthesis and inhibiting lipid oxidative degradation.

Objective: Herbal prescriptions hold significant importance in Traditional Chinese Medicine (TCM) diagnosis and treatment, embodying millennia of clinical case summaries and wisdom. Despite numerous proposed methods for herbal prescription recommendation (HPR), significant challenges persist due to the lack of comprehensive clinical data, particularly regarding the relationships between symptoms and herbs. This scarcity poses considerable hurdles for effective HPR modeling.

Methods: In this study, we introduced a novel herbal prescription recommendation framework with cross-domain neural collaborative filtering (termed PresRecCDL). The cross-domain learning mechanism is introduced to learn the noise-reduced cross-domain features of herbs and symptoms in the unified space, which alleviated the sparsity of data, and the neural collaborative filtering is utilized to carry out prescription recommendations.

Results: Comprehensive experiments demonstrate the superiority of the proposed PresRecCDL model over the SOTA model. The effectiveness of each module in PresRecCDL and model robustness are validated by the ablation and hyper-parameter tuning experiments, respectively. The case study based on network pharmacology further validates the effectiveness of the proposed approach, particularly its scientific rigor and feasibility at the molecular mechanism level.

Conclusion: This study contributes to enhancing the performance of the HPR model, ultimately benefiting the efficiency and precision of clinical treatment.