Bioactive dicaffeoylquinic acid-enriched callus extract of Weigela subsessilis inhibits TNF-α/IFN-γ-induced keratinocyte inflammation via MAPK and NF-κB pathways

Xanthium strumarium L. extract attenuates TNF-α/IFN-γ- stimulated inflammation and promotes hyaluronan production on HaCaT keratinocytes

The findings demonstrate that the anti-inflammatory and hyaluronan-producing properties of XsE may contribute to the regulation of epidermal inflammatory responses and skin barrier-associated functions.

Apigetrin ameliorates psoriatic inflammation and skin barrier dysfunction via NF-κB/STAT3 pathway in epidermal and dermal cell models

Ethanolic Extract of Sophora moorcroftiana Seeds Attenuates LPS-Induced Inflammation and Oxidative Stress in RAW 264.7 Macrophages via Modulation of the p62/Keap1/Nrf2 Signaling Pathway

The ethanolic extract of SMS attenuated LPS-induced inflammatory and oxidative stress responses in RAW 264.7 macrophages, suggesting effects may be associated with the suppression of inflammatory mediator production, reduction in the cellular oxidative stress burden and modulation of proteins involved in cellular stress responses and antioxidant defense.

Isorhamnetin from Lycium ruthenicum Murr. exhibits anti-inflammatory and anticancer activities in vitro via regulation of oxidative stress, mitochondrial function, and AKT signaling

Black goji berry (Lycium ruthenicum Murr.) has been recognized for its immune-regulating and anti-cancer potentials, but its key active components and underlying mechanisms remain unclear. Here, we applied LC–MS/MS to characterize the metabolite profile of L. ruthenicum and performed in vitro assays to evaluate its anti-inflammatory and anti-cancer activities. A total of 149 metabolites were identified, with organic acids, carbohydrates, and amino acid derivatives as the dominant components. Isorhamnetin was identified as a representative flavonoid. In LPS-stimulated Calu3 cells, isorhamnetin reduced the secretion and mRNA expression of pro-inflammatory cytokines (IL-6, TNF-alpha, IL-1beta). In cancer cells, isorhamnetin induces ROS accumulation, DNA damage, mitochondrial dysfunction, and caspase-3-dependent apoptosis, with modulation of the AKT signaling pathway. These findings suggest that isorhamnetin may contribute to the anti-inflammatory and anti-cancer effects of L. ruthenicum observed in vitro, providing preliminary experimental evidence for its potential as a functional food ingredient. However, this study is limited by the use of a single cell line (Calu3) and the absence of in vivo validation and pharmacokinetic evaluation; further studies are needed to confirm these observations.

Methanolic extracts of Amaranthus spinosus (Linn.) mitigate TAA-Induced hepatic fibrosis through modulation of inflammatory cytokines and profibrotic signalling.

BACKGROUND Persistent oxidative stress disrupts intrahepatic immune homeostasis, leading to cytokine dysregulation and fibrogenic progression in the liver. This study investigated the immunomodulatory and antifibrotic effects of methanolic extracts of Amaranthus spinosus (leaf, stem, and root) in a thioacetamide (TAA)-induced murine model of hepatic fibrosis. METHODS Swiss albino mice were administered TAA (150 mg/kg, intraperitoneally, thrice weekly for 8 weeks) to induce fibrosis, followed by oral treatment with plant extracts (250 mg/kg) for 15 consecutive days. Hepatocyte-specific cytokine expression (IL-6, TNF-α, IL-12, TGF-β, and IL-10) was evaluated by flow cytometry and quantitative real-time PCR, and immunohistochemistry was used to assess COX-2 and iNOS expression. RESULTS TAA administration resulted in significant upregulation of pro-inflammatory (IL-6, TNF-α, IL-12) and profibrotic (TGF-β) cytokines, along with elevated IL-10 expression, indicating dysregulated immune homeostasis. Extract treatment significantly attenuated (p < 0.01) these alterations in a fraction-dependent manner, with the root extract exhibiting the highest efficacy, restoring cytokine levels to near physiological baseline. These findings were corroborated at the transcriptional level by qPCR. Additionally, extract-treated groups showed significant downregulation of COX-2 and iNOS expression, reflecting reduced oxidative and nitrosative stress. In contrast, TAA withdrawal alone, or in combination with the vehicle control, failed to effectively normalize inflammatory markers. CONCLUSIONS Collectively, these results demonstrate that A. spinosus exerts potent antifibrotic activity by modulating hepatocyte-driven cytokine networks and suppressing redox-sensitive inflammatory pathways. The root extract, in particular, shows strong therapeutic potential as a multi-target agent capable of disrupting the inflammation-fibrosis axis in chronic liver injury.

Sphallerocarpus gracilis Polyphenols Alleviate DSS-Induced Colitis by Remodeling Gut Microbiota and Inhibiting the AGE-RAGE/HMGB1 Pathway

As a traditional Tibetan medicine and health food, the fleshy roots of Sphallerocarpus gracilis were adopted to extract polyphenol powder(PP) in this research. Using a DSS-induced colitis mouse model combined with multi-omics analysis and experimental validation, we explored the protective effects and molecular mechanisms of PP against intestinal inflammation. PP mitigated colitis-related symptoms in a dose-dependent manner, inhibited pro-inflammatory cytokines and dose-dependently reversed elevated IL-10 levels to BC group. Multi-omics data revealed that PP intervention was associated with gut microbiota remodeling, enrichment of Akkermansia muciniphila, restoration of bacterial–fungal homeostasis, and improvement of tryptophan and biotin metabolism. By suppressing HMGB1 and RAGE expression, PP blocked the AGE-RAGE-mediated inflammatory cascade. In addition, PP maintained intestinal mucosal integrity through goblet cell protection, MDA reduction, and the regulation of BAX/Bcl-2, MMP3 and MMP9. Overall, PP relieves UC by regulating gut microecology, host metabolism and the AGE-RAGE pathway, which supports the translational potential of natural polyphenols for inflammatory bowel disease treatment as a gut microecological modulator.