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Traditional Chinese medicine (TCM) is an entirely coherent system, with internal logic and consistency of thought and practice. Though TCM has a long history, it is not easily accepted by Western medicine due to its theoretical and conceptual complexity. TCM nutrition is an ancient but burgeoning discipline, and its main goal is to use food as a means to achieve balance and harmony within the body. Compared with modern nutrition, it has unique beneficial concepts, such as the holism, diet suggestions based on syndrome differentiation, the idea that the spleen–stomach is the “root” of post-heaven, and the homology of medicine and food. Until today, it is difficult to evaluate whether TCM nutrition could play a major role in the treatment of various diseases. The limitations mainly include: the scope of application is limited, lack of evidence-based research, and the constitution differentiation need the cooperation of clinicians of TCM. In contemporary China, the inheritance, innovation, and broadening the scope of applications of TCM nutrition is very important. The government should establish a system in which TCM nutrition and modern nutrition coexist, and perform higher specialist training for dietitians of TCM. Moreover, TCM nutrition should integrate the research methods of modern nutrition, and involve adjustment to target populations, the formulation of age-specific nutrition principles, and an emphasis on the research and development of nutritional food, thus fully demonstrating the advantages and characteristics of TCM nutrition.

This study aimed to isolate, prepare and identify the main flavonoids from a standardized Smilax glabra flavonoids extract (SGF) using preparative HPLC, MS, 1H NMR and 13C NMR, determine the contents of these flavonoids using UPLC, then compare their pharmacological activities in vitro. We obtained six flavonoids from SGF: astilbin (18.10%), neoastilbin (11.04%), isoastilbin (5.03%), neoisoastilbin (4.09%), engeletin (2.58%) and (−)-epicatechin (1.77%). The antioxidant activity of six flavonoids were evaluated by determining the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical and 2,2′-Azinobis (3-ethylbenzothiazoline-6-sulphonic acid) diammonium salt (ABTS+) radical scavenging activity and ferric reducing antioxidant power (FRAP). In addition, the anti-inflammatory activity of six flavonoids were evaluated by determining the production of cytokines (IL-1β, IL-6), nitric oxide (NO) using enzyme linked immunosorbent assay and the NF-κB p65 expression using Western blotting in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The results showed that (−)-epicatechin, astilbin, neoastilbin, isoastilbin and neoisoastilbin had strong antioxidant activities, not only in DPPH and ABTS+ radicals scavenging capacities, but in FRAP system. Furthermore, all the six flavonoids could significantly inhibit the secretion of IL-1β, IL-6, NO (p < 0.01) and the protein expression of NF-κB p-p65 (p < 0.01) in LPS-stimulated RAW264.7 cells. This study preliminarily verified the antioxidant and anti-inflammatory activities of six flavonoids in S. glabra.

Chrysanthemum morifolium cv. Hang-ju (HJ) is considered as a healthy food supplement for a long time in Asia. But until now, there are few reports on the biological activity of HJ leaves, which is the main by-products of HJ. In this study, HJ leaves was extracted by water, ethanol and water: ethanol (30: 70), respectively. The results showed that the total polyphenol content of water extract, hydroalcoholic extract and ethanol extract was 75.1 ± 6.9 mg GAE/g, 162.2 ± 5.6 mg GAE/g and 128.5 ± 1.9 mg GAE/g, respectively. However, the ethanol extract has the highest antibacterial activity against the tested strains with a MIC of 0.25 mg/mL compared to water extract (MIC > 8.0 mg/mL) and ethanol extract (MIC = 0.50 mg/mL). The essential oil was extracted from HJ leaves by water distillation (0.5%), which showed higher antibacterial effect on gram-positive bacteria (MIC = 0.125 mg/mL) than ethanol extract. GC–MS was used for the preliminary identification of essential oil composition. The compound (1S,4aS,7R,8aS)-1,4a-dimethyl-7-(prop-1-en-2-yl)decahydronaphthalen-1-ol was first identified from HJ and found to be the most dominant compound. Furthermore, essential oil can significantly deform cell morphology and damage cell wall structure, which was confirmed by LIVE/DEAD® BacLight Viability Kit and scanning electron microscopy observations. The mentioned findings indicated that HJ leaves could be utilized as a natural additive in food industry with significant antimicrobial potential.

Background Mitochondrial fission and fusion are dynamic and highly regulated processes that are essential for maintaining cellular homeostasis. These processes are regulated by core proteins, including dynamin-related protein 1 (DRP1), fission 1 protein (FIS1), mitochondrial fission factor (MFF), mitofusin 1 (MFN1), mitofusin 2 (MFN2), and optic atrophy 1 (OPA1), which ensure proper mitochondrial function and integrity. Main body An imbalance in fission and fusion can lead to excessive production of ROS, mtDNA release, and alterations in immune cell phenotypes. These disruptions compromise mitochondrial integrity, redox balance, and metabolic adaptability, ultimately activating inflammatory signaling pathways and triggering immune dysregulation. Restoring mitochondrial dynamics has emerged as a promising therapeutic strategy to mitigate these disruptions. A growing number of evidence indicates that small-molecule modulators, natural compounds, genetic interventions, chemical drugs, and mitochondria-targeted nanoformulations hold great potential for re-establishing mitochondrial homeostasis and suppressing inflammation. This review systematically elucidates the molecular mechanisms by which mitochondrial fission and fusion regulate inflammation, summarizes current therapeutic advances, and discusses translational perspectives and future challenges in this rapidly evolving field. Conclusions Modulating mitochondrial dynamics is a promising therapeutic strategy for inflammation, but its clinical translation still faces many challenges. Future research should focus on optimizing mitochondrial dynamic modulation strategies and evaluating their long-term efficacy and safety.

The prevalence of type 2 diabetes mellitus (T2DM) continues to rise, and traditional models fail to fully explain its pathogenesis, particularly the frequent co-occurrence of T2DM with mental health disorders. Based on a systematic integration of epidemiological and molecular biological studies, this review organises existing evidence into a \"psychological stress-sleep disturbance-food addiction\" triangular framework, drawing together observations that have mostly been discussed in isolation. In this model, the three factors form a self-perpetuating vicious cycle through bidirectional interactions, which may synergistically amplify the risk of both T2DM and comorbid mental health conditions via shared molecular pathways. Mechanistically, the model operates through three tiers of pathological amplification: central drive (HPA axis and autonomic imbalance), peripheral effects (glucocorticoid resistance-driven inflammation and metabolic dysregulation), and tissue damage (insulin resistance and β-cell dysfunction). Glucocorticoid resistance serves as the key link connecting central overdrive to amplified peripheral inflammation. The same neuroendocrine and inflammatory pathways are implicated in mood and cognitive disturbances, suggesting a biological basis for the mental-metabolic comorbidity observed clinically. This framework provides an integrated understanding of how psychosocial and dietary factors converge on common biological targets and offers a theoretical foundation for developing integrated nutritional and psychological prevention strategies.

Lipids play an important role in the regulation of cell life processes. Although there are various lipid detection methods, Raman spectroscopy, a non-invasive technique, provides the detailed chemical composition of lipid profiles without a complex sample preparation procedure and possesses greater potential in basic biology, clinical diagnosis and disease therapy. In this review, we summarized the characteristics and advantages of Raman-based techniques and their primary contribution to illustrating cellular lipid metabolism. [Display omitted] •Raman spectroscopy is a crucial tool in basic biology, clinical diagnosis and disease therapy.•Raman spectroscopy has great advantages in studying lipids in cells, including lipid metabolism.•Raman spectroscopy will evolve towards high-throughput, real-time analysis, integrating multimodal imaging and AI.

Background/Objectives: Gouty arthritis (GA) is an inflammatory disease caused by increased purine metabolism. The limitations of current anti-GA therapies remain a major challenge. Astilbin, the main flavonoid in Smilax glabra Roxb., was found to exert potential anti-GA effects in our previous study. Methods: In this study, a mouse model of monosodium urate (MSU)-induced arthritis and an inflammatory model using mouse bone marrow-derived macrophages (BMDMs) were established. Results: Our data showed that astilbin reduced MSU-induced joint swelling and inflammatory infiltration in mice, restored lipopolysaccharide (LPS)/MSU-induced reductions in cell viability, and inhibited the expression levels of inflammatory factors IL-1β, IL-6 and TNF-α. Further studies showed that astilbin significantly reduced MSU-induced increases in NLRP3 and P-p65 protein levels, as well as the expression of ASC, P-IKKα, P-IκBα, and cleaved-caspase-1. Conclusions: This study suggests that astilbin may be a promising natural product for the treatment of GA by inhibiting the activation of the NLRP3 inflammasome and NF-κB signaling pathway.

Gouty arthritis (GA) is a frequent inflammatory disease characterized by pain, swelling, and stiffness of joints. Neoastilbin is a flavonoid isolated from the rhizome of Smilax glabra, which possesses various anti-inflammatory effects. However, the mechanism of neoastilbin in treating GA has not yet been clarified. Thus, this study was to investigate the protective effects of neoastilbin in both monosodium urate (MSU) stimulated THP-1-derived macrophages and the animal model of GA by injecting MSU into the ankle joints of mice. The levels of key inflammatory cytokines in MSU stimulated THP-1-derived macrophages were detected by enzyme-linked immunosorbent assay (ELISA) kits. Protein expressions of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasome pathways were further detected by Western blotting. In addition, swelling degree of ankle joints, the levels of inflammatory factors, infiltration of inflammatory cells and the expressions of related proteins were determined. Swelling degree and histopathological injury in ankle joints of MSU-injected mice were significantly decreased after being treated with neoastilbin. Moreover, neoastilbin significantly diminished the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), suppressing the activation of NF-κB and NLRP3 inflammasome pathways in both MSU stimulated THP-1-derived macrophages and the mouse model of GA. In summary, neoastilbin could alleviate GA by inhibiting the NF-κB and NLRP3 inflammasome pathways, which provided some evidence for neoastilbin as a promising therapeutic agent for GA treatment.

Background: Polygonatum sibiricum (PS), a perennial herbaceous plant belonging to the Liliaceae family, is widely distributed in China and other East Asian countries. PS has been used as food and medicine for thousands of years, and its rhizomes are rich in Polygonatum sibiricum polysaccharides (PSP), which exhibit various bioactivities, yet their structural features and therapeutic mechanisms against ulcerative colitis (UC) remain unclear. Methods: A homogeneous polysaccharide, PSP-1b (57.45 kDa), was isolated from the rhizomes of PS via ion-exchange and gel filtration chromatography and structurally characterized using chromatographic and spectroscopic methods. In vivo, its effects were evaluated in a dextran sulfate sodium (DSS)-induced mouse model of UC, while in vitro mechanisms were explored using macrophages stimulated with lipopolysaccharide (LPS) and neutrophil extracellular traps (NETs). Results: PSP-1b was identified as a neutral polysaccharide with minimal branching. Its primary structural backbone was largely composed of →4)-β-D-Galp-(1→ residues. A portion of these backbone residues was substituted at the O-6 position by side chains primarily composed of β-D-Galp-(1→ units. In vivo, PSP-1b significantly alleviated DSS-induced colitis by reducing inflammatory cytokine secretion, suppressing colonic macrophage infiltration, and reversing neutrophil extracellular traps (NETs) deposition. In vitro, PSP-1b directly interacted with TLR4, inhibited the MAPK/NF-κB signaling pathway, and attenuated LPS- and NET-induced macrophage polarization and inflammation. Conclusions: PSP-1b as a promising candidate for functional foods or therapeutic agents targeting inflammatory bowel disease.

Lead (Pb) is an important environmental pollutant. Oxidative stress and the inflammatory response have been postulated as mechanisms involved in lead-induced renal damage. Smilax glabra Roxb. has been used for treatment of heavy-metal poisoning in China for 500 years. We investigated S. glabra flavonoids extract (SGF) could attenuate lead acetate-induced nephrotoxicity in weaning rats and human embryonic kidney (HEK)-293 cells, and investigated the possible mechanisms. Compared with Pb exposed group of weaning rats, SGF could significantly promote lead excretion in the blood and kidney, and increase the content of the renal-function indicators blood urea nitrogen, serum uric acid, and serum creatinine. SGF could improve the glomerular filtration rate (GFR) and histologic changes in the kidneys of weaning rats exposed to Pb. SGF could also reduce lead-induced cytotoxicity, improve DNA damage-induced apoptosis and cleaved caspase-3-mediated apoptosis in HEK-293 cells stimulated with Pb. SGF significantly increased the activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase and catalase, and decreased excessive release of reactive oxygen species (ROS) and malondialdehyde in the kidneys of the weaning rats and in HEK-293 cells. The antioxidant mechanism of SGF related to activation of the Kelch-like ECH-associated protein 1/nuclear-factor-E2-related factor 2/hemeoxygenase-1(Keap1/Nrf2/HO-1) pathway. SGF could inhibit secretion of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α induced by Pb in vivo and in vitro . The anti-inflammatory mechanism of SGF related to inhibition of ROS and pro-inflammatory cytokines triggered the nuclear factor-kappa B (NF-κB) pathway through blockade of inhibitors of I-κB degradation, phosphorylation of NF-κB p65, and nuclear translocation of p65. Our findings indicate that SGF could be a natural antioxidant and anti-inflammatory agent for treating lead-induced nephrotoxicity.