Qi stagnation and blood stasis (QSBS) is a core pathogenesis in traditional Chinese medicine (TCM), with clinical correlates to multifactorial modern diseases involving inflammation, microvascular occlusion, oxidative injury, and neuroendocrine-immune dysregulation. This review comprehensively summarizes the flavonoid constituents from Qi- and Blood-regulating TCM herbs and examines the pharmacological mechanisms that may contribute to their efficacy against QSBS. A comprehensive literature search was conducted using PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) databases, focusing on studies of the chemical constituents and pharmacology of flavonoids related to “activating blood, resolving stasis, regulating Qi, and dissipating masses.” Flavonoids, representative bioactive constituents of Qi- and Blood-regulating TCMs (e.g., Salvia miltiorrhiza and Ligusticum chuanxiong ), have shown potential for QSBS intervention due to their polypharmacological profiles. Key flavonoids such as hydroxysafflor yellow A, quercetin, luteolin, hesperidin, and naringenin have been reported to act through multiple signaling pathways (NF-κB, Nrf2, and MAPK), covering antioxidative stress, anti-inflammation, microcirculation restoration, and platelet inhibition. However, most mechanistic evidence is derived from isolated compounds and preclinical models, and human pharmacokinetic data remain limited. Flavonoids represent one important class of bioactive constituents that may contribute to QSBS intervention. Their coordinated regulation of multiple cascades is consistent with the TCM doctrine of “Qi-blood co-regulation.” This review provides a theoretical basis for the development of flavonoid-based therapeutics and their potential clinical application. Because direct evidence linking flavonoids to measurable neuroendocrine and neuroimmune endpoints in QSBS remains scarce, the neuro-vascular-immune interpretation of “Qi” is presented here as a hypothesis-generating framework rather than an established mechanism.
Objective This study aimed to comprehensively compare the efficacy, safety, and underlying molecular mechanisms of fucoxanthin, a natural carotenoid, with those of retinol, the gold-standard anti-aging agent, in key skin cell models. The objective was to evaluate the potential of fucoxanthin as a safer, anti-inflammatory alternative to retinol, focusing on retinoid activity, anti-inflammatory effects, extracellular matrix synthesis, and global transcriptomic changes. Methods High-purity fucoxanthin was extracted from the diatom Phaeodactylum tricornutum and characterized using spectral analysis, HPLC, and NMR. In vitro assessments in HaCaT keratinocytes and human dermal fibroblasts (HDFs) included cytotoxicity (CCK-8 assay), gene expression of retinoid targets (RARG, RBP1), inflammatory cytokines (IL-6, IL-8, TNF-α), and extracellular matrix components (COL1A1, COL3A1, ELN) via qPCR. A comprehensive transcriptome analysis (RNA-Seq) was performed to elucidate differential pathway regulation. Results Fucoxanthin exhibited significantly lower cytotoxicity than retinol in both cell lines. It effectively upregulated RARG and RBP1 gene expression, indicating selective transcriptional activity on retinoid-related targets. Crucially, fucoxanthin potently suppressed LPS-induced pro-inflammatory cytokine expression, whereas retinol showed inconsistent inhibition and even exacerbated TNF-α expression. Conclusion Fucoxanthin functions as a high-efficacy, low-irritancy compound that shares certain functional similarities with retinol, including the modulation of retinoid-related gene expression and stimulation of collagen synthesis, while demonstrating superior safety and anti-inflammatory properties. It delivers comparable anti-aging benefits by stimulating collagen synthesis and engaging retinoid signaling, but crucially diverges from retinol by concurrently activating robust anti-inflammatory and homeostatic mechanisms.
Akkermansia muciniphila is a mucin-degrading member of the human gut microbiota that has attracted considerable interest because of its associations with intestinal barrier integrity, immune regulation, and metabolic homeostasis. Although direct supplementation and dietary manipulation have been investigated, increasing evidence indicates that medicinal plants, herbal preparations, dietary phytochemicals, and plant-derived carbohydrates may also modify its abundance or ecological activity. This narrative review critically examines how medicinal plants and plant-derived compounds modulate A. muciniphila and evaluates the biological mechanisms, associated host outcomes, evidence strength, and translational relevance of these interactions. Literature was identified from PubMed/MEDLINE, Google Scholar, and additional bibliographic sources using combinations of terms related to A. muciniphila , gut microbiota, medicinal plants, herbal medicine, phytochemicals, polyphenols, polysaccharides, prebiotics, intestinal barrier function, inflammation, obesity, diabetes, and metabolic health. The present article is a narrative review and therefore does not claim a formal systematic-review or meta-analytic methodology. Relevant evidence was synthesized according to intervention type, model, mechanism, and evidence level. Preclinical studies summarized in the source literature indicate that several medicinal plants and plant-derived constituents including Abelmoschus manihot flavones, Agave salmiana saponins, Antrodia cinnamomea , Artemisia asiatica , berberine, Boswellia serrata constituents, Bofutsushosan, Gastrodia elata polysaccharides, rhubarb, Rhizoma Coptidis alkaloids, Platycodon grandiflorus, andrographolide, diosmin, and green tea can increase A. muciniphila abundance or create an intestinal environment favorable to its persistence. Proposed mechanisms include enhanced mucus production, epithelial-barrier support, SCFA generation, microbial cross-feeding, bile-acid signaling, and modulation of inflammatory pathways. Human evidence is substantially more limited and heterogeneous. Medicinal plants and plant-derived compounds represent promising candidates for microbiota-directed strategies involving A. muciniphila , but current evidence is predominantly preclinical. Changes in A. muciniphila abundance should not be interpreted as proof of causality, therapeutic efficacy, or safety. Standardized botanical preparations, strain-aware microbiome analyses, mechanistic studies, and adequately powered clinical trials are required before clinical translation.
Objectives In the Li ethnic minority region in Hainan, China, the leaves of Nauclea officinalis are traditionally used as an ingredient in herbal teas, typically prepared by boiling in water. These teas are believed to be effective in alleviating symptoms associated with pulmonary diseases. However, a lack of scientific understanding regarding their mechanisms of action has significantly hindered the further development and utilization of N. officinalis leaves. This study aims to elucidate the mechanism by which N . officinalis leaves alleviate the symptoms of pulmonary diseases, thereby filling the gap in scientific research on this medicinal herb and providing support for its subsequent development and application. Methods This study integrated metabolomics and network pharmacology approaches to screen and analyze the active components in N. officinalis leaves that are closely associated with pneumonia. The findings were subsequently validated through molecular docking techniques and in vitro cellular experiments. Results Using metabolomics technology, the active components in N. officinalis leaves closely associated with pneumonia-related targets were screened. Network pharmacology analysis revealed that IL-6, STAT3, and TNF-α serve as key proteins playing central regulatory roles. In vitro experiments demonstrated that N. officinalis leaves significantly reduce the levels of the inflammatory cytokines IL-6, TNF-α, and IL-1β, suggesting that they may exert therapeutic effects on pneumonia by modulating the IL-6/STAT3 signal pathway. Conclusion The aqueous extract of N. officinalis leaves may exert anti-inflammatory effects in vitro by modulating the IL-6/STAT3 signaling pathway, thereby providing a preliminary theoretical and experimental basis for its further development. However, its in vivo efficacy in treating pneumonia, relative anti-inflammatory potency, and direct validation of STAT3 phosphorylation levels remain to be confirmed in further studies.
Objectives Stingless bee honey (SBH) has reported anticancer activity that is generally attributed to its phenolic acids and flavonoids. We previously described the synthesis, characterization, and wound-healing activity of SBH-loaded alginate nanoparticles (H-ALG NPs). Here, we evaluated the in vitro cytotoxic and anti-migratory activities of H-ALG NPs against cancer cell lines and their effect on the expression of inflammatory and immune-related genes in cancer cells and in macrophage-like cells. Methods Cytotoxicity of H-ALG NPs, crude SBH, and free alginate nanoparticles (free ALG NPs) was assessed by MTT assay in four cancer cell lines (MCF-7, MDA-MB-231, A549, U87) and in normal human dermal fibroblasts (HDFa). Cell migration was evaluated by in vitro scratch assay. Transcript levels of inflammatory and immune-related genes were measured by quantitative PCR (qPCR) in cancer cells and in PMA-differentiated, LPS-activated THP-1 macrophage-like cells. Results H-ALG NPs showed significantly greater cytotoxicity than crude SBH against the four cancer cell lines (P < 0.01), with IC 50 values of 30.70 ± 3.44 µg/mL (MCF-7), 71.23 ± 5.17 µg/mL (U87), 73.59 ± 7.31 µg/mL (A549), and 84.45 ± 8.81 µg/mL (MDA-MB-231). Viability of HDFa fibroblasts was not reduced below 50% up to 1000 µg/mL. In the scratch assay, H-ALG NPs reduced wound closure more than crude SBH or free ALG NPs. By qPCR, H-ALG NPs increased TNF and IL-6 transcripts in cancer cells but produced a smaller increase in HDFa cells. In LPS-activated THP-1 macrophage-like cells, H-ALG NPs lowered the transcript levels of TNF, IL-6, TLR4, IRAK1, IDO1, FOXP3 , and TFRC , and raised IL-10, PTGES, and CD39 . Conclusion H-ALG NPs showed selective in vitro cytotoxicity toward cancer cells relative to a normal fibroblast line, reduced scratch closure, and altered the expression of selected inflammatory and immune-related genes in cancer cells and in macrophage-like cells. Together with our earlier wound-healing findings, the results support further preclinical evaluation of H-ALG NPs.
