Context Atopic dermatitis is a chronic inflammatory skin disorder characterized by epidermal barrier dysfunction and dysregulated type 2 helper T cell (Th2)-mediated immune responses. Erigeron annuus (L.) Desf. is traditionally used for inflammatory conditions, but its effects on atopic dermatitis remain unclear.Objective This study evaluated the protective effects of E. annuus aqueous extract (EA) and associated mechanisms.Materials and methods Atopic dermatitis-like lesions were induced in 5-week-old female BALB/c mice by repeated epicutaneous ovalbumin (OVA) sensitization, and EA was orally administered for six weeks. Epidermal barrier function, histopathology, immunoglobulins, cytokines, and mitogen-activated protein kinase (MAPK) signaling were evaluated. Pyromeconic acid (PA), a representative constituent of EA, was examined in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages.Results EA attenuated dermatitis-like lesions and reduced dermatitis scores in OVA-sensitized mice. EA decreased transepidermal water loss, increased skin hydration, restored filaggrin expression, and reduced epidermal and dermal thickening, mast cell infiltration, CD4+/CD8+ T-cell accumulation, splenomegaly, serum total and OVA-specific IgE, and skin interleukin-4 and interleukin-13 levels. EA also reduced extracellular signal-regulated kinase and p38 phosphorylation and interleukin-1β expression in dorsal skin. PA suppressed MAPK activation and inflammatory mediator expression in LPS-stimulated macrophages.Discussion and conclusion EA attenuated OVA-induced atopic dermatitis-like inflammation in association with improved epidermal barrier function, reduced Th2-associated immune responses, and attenuated MAPK signaling. PA showed anti-inflammatory activity in vitro, although its contribution to the in vivo effects of EA remains to be established. EA warrants further investigation as a plant-derived candidate for complementary intervention in atopic dermatitis.
Context BMSC senescence is associated with osteoporosis progression. Polygonatum sibiricum polysaccharide (PSP) shows potential anti-senescence activity, but its effects on bone marrow mesenchymal stem cells (BMSCs) remain unclear.Objective To investigate the protective effects and molecular mechanisms of PSP against tert-butyl hydroperoxide (TBH)-induced senescence in BMSCs.Materials and methods Senescence was induced in primary rat BMSCs with TBH, followed by PSP intervention. Viability was assessed using the Cell Counting Kit-8 assay, while senescence-associated β-galactosidase, alkaline phosphatase, and Oil Red O staining assessed senescence and osteogenic/adipogenic differentiation. Ferritinophagy-associated proteins (NCOA4, FTH1, and LC3) and intracellular Fe2+ were quantified using western blot, immunofluorescence, and FerroOrange staining. Mitochondrial function was evaluated using MitoSOX and JC-1 assays and ATP quantification. Cytosolic mtDNA accumulation and the cGAS–STING pathway were assessed using immunofluorescence colocalization, quantitative polymerase chain reaction, and Western blotting. NCOA4 involvement was examined using an NCOA4-overexpressing lentiviral vector.Results PSP concentration-dependently attenuated TBH-induced senescence phenotypes in BMSCs, partially restored osteogenic differentiation, and reduced adipogenic differentiation. PSP downregulated NCOA4 expression, attenuating ferritinophagy-associated changes and intracellular Fe2+ accumulation. Reduced Fe2+ accumulation preserved mitochondrial membrane potential, reduced mitochondrial reactive oxygen species generation, and reduced cytosolic mtDNA accumulation, alongside attenuated cGAS–STING signaling. Lentiviral overexpression of NCOA4 attenuated the protective effects of PSP on mitochondrial homeostasis and cGAS–STING pathway suppression.Discussion and conclusions PSP may attenuate BMSC senescence by suppressing NCOA4-mediated ferritinophagy, thereby preserving mitochondrial homeostasis and inhibiting cGAS–STING signaling. These findings provide a rationale for further investigation of PSP as a potential therapeutic strategy for osteoporosis-associated BMSC dysfunction.
Context Turmeric (Curcuma longa L. Zingiberaceae) is a highly valued botanical medicine worldwide and has emerged as among the best-selling herbal products in North America.Objective Presented an ethnobotanical record of turmeric use to present a context for this edition on turmeric.Methods Information was primarily compiled from online sources including PubMed, Web of Science, Google Scholar, and Science Direct using ‘turmeric’, ‘curcuma’, and ‘curcuma longa’ as search terms; No time limit was specified. The primary goal was to mine ethnobotanical literature regarding turmeric use of various cultures. Online searches were augmented by hardcopy searches of ethnobotanical, and pharmacognosy literature from the first century.Results and conclusion Turmeric is used in an array of preparations. It is listed among the top ten spices in the world and is used as a dye, medicine, object of cultural and religious significance, and coloring agent. Turmeric is used in African, Ayurvedic, Korean, Malaysian, Siddha, Chinese, Persian, Unani, and Western herbal traditions though India remains the largest producer and consumer of turmeric. Turmeric is universally used to support healthy gastrointestinal, circulatory, respiratory, and renal systems. The treatment of jaundice was one of turmeric’s primary historical indications. In combination with other botanicals, turmeric is used for treating almost any condition. Following is an ethnobotanical review of its traditional uses and select botanical pharmacognostic characteristics used for ensuring authenticity of raw material, including a discussion of some of the most common adulterants of turmeric products.
Context Icariin (ICA), a prenylated flavonol glycoside from Epimedii Folium, has been investigated in experimental models relevant to atherosclerosis, myocardial infarction, and ischemic tissue injury.Objectives This review evaluates experimental evidence on ICA in atherosclerotic plaque biology, post-myocardial infarction remodeling, myocardial ischemia-reperfusion injury, and cerebral ischemic injury.Methods PubMed and the Web of Science Core Collection were searched from database inception to 19 August 2026, and studies were selected using predefined eligibility criteria. Targeted searches also covered pharmacokinetics, metabolism, toxicology, botanical source, quality control, formulation, and delivery.Results In atherosclerosis models, ICA reduced endothelial inflammatory activation, macrophage lipid uptake, vascular smooth muscle cell (VSMC) proliferation and migration, and lesion burden. Several mechanistic links were tested using pharmacological or genetic perturbation. In vivo studies primarily characterized lesion burden and circulating lipids, with less direct assessment of plaque composition and stability. Post-myocardial infarction and ischemic injury studies reported reductions in fibrosis and ischemic tissue injury, together with reduced mitochondrial injury and changes in inflammatory signaling, apoptosis, and ferroptosis-related processes. Functional improvement was also reported in several models. Few studies measured parent ICA or metabolite concentrations in plaque, myocardium, or brain in the same experiments in which pathological outcomes were assessed.Conclusions Future studies should quantify parent ICA and active metabolites in diseased tissues while assessing plaque composition and stability in the same experiments, so that vascular effects can be related to measured in vivo exposure.
