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

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

Inflammatory skin diseases (ISDs) involve chronic inflammation and excessive cytokine production, compromising skin function. Weigela subsessilis exhibits antioxidant and anti-inflammatory properties, yet its callus-derived bioactive potential remains unexplored. This study evaluates WS callus extract (WSCE) in TNF-α and IFN-γ (T+I)-induced keratinocytes, identifying key metabolites and underlying molecular mechanisms for potential ISD treatment. WSCE (6.25–25 μg/mL) substantially suppressed T+I-induced production of pro-inflammatory mediators (MCP-1, RANTES, MDC, CTACK, IL-6, and IL-8) and inhibited MAPK and NF-κB signaling pathways, but not the Akt pathway, underscoring its regulatory potential in inflammatory conditions. UHPLC-MS/MS and HPLC-DAD analyses identified chlorogenic acid (CGA; 30.1 mg/g) and three dicaffeoylquinic acids (DCQAs; 3,5-DCQA, 6.1 mg/g; 4,5-DCQA, 4.5 mg/g; 3,4-DCQA, 0.6 mg/g) as the primary bioactive compounds in WSCE. Functional evaluations showed that 3,5-DCQA and 4,5-DCQA considerably reduced MCP-1 levels (by 11.9%–32.7%), whereas CGA and 3,4-DCQA effectively diminished IL-8 levels (by 44.2%–55.6%). This study highlights WSCE as a potential anti-dermatitis agent, suppressing pro-inflammatory mediators (MCP-1, RANTES, MDC, CTACK, IL-6, IL-8) in T+I-stimulated keratinocytes via MAPK and NF-κB regulation. These findings underscore the therapeutic potential of callus-derived extracts and position WSCE as a promising candidate for ISD management.

Rosmarinus officinalis ethanol extract suppresses sebocyte lipid accumulation and exhibits antioxidant, antiinflammatory, and anti-cutibacterium acnes activities

Rosmarinus officinalis ethanol extract (REE) was evaluated for its potential anti-acne activity by assessing its antioxidant, anti-sebogenic, anti-inflammatory, and antibacterial properties. Phytochemical characterization showed that REE contained 144.66 ± 2.43 mg GAE/g REE of total phenolic content and 25.55 ± 0.42 mg/g REE of rosmarinic acid. REE exhibited potent DPPH radicalscavenging activity (IC₅₀=62.96 μg/mL) and markedly reduced intracellular reactive oxygen species (ROS) in HaCaT keratinocytes. In SEB-1 sebocytes, REE inhibited linoleic acid-induced sebum synthesis by up to 81.02% without inducing cytotoxicity, as confirmed by Oil Red O and Nile Red staining. Furthermore, REE significantly attenuated Cutibacterium acnes lysate-induced inflammatory responses in HaCaT cells by reducing the secretion of pro-inflammatory cytokines interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α). REE also demonstrated dose-dependent antibacterial activity against C. acnes, as evidenced by progressively increased inhibition zone diameters with higher extract concentrations. Western blot analysis revealed that REE downregulated peroxisome proliferatoractivated receptor gamma (PPAR-γ) and sterol regulatory element-binding protein 1 (SREBP-1), key transcriptional regulators of lipid biosynthesis. Collectively, these findings suggest that REE may alleviate acne-related pathological processes by reducing sebocyte lipid accumulation through the downregulation of PPAR-γ and SREBP-1 expression, while also exerting antioxidant, antiinflammatory, and antibacterial effects.

Black mulberry fruit extract attenuates valproic acid-induced toxicity by enhancing antioxidant defenses in FaO cells.

Findings indicate that black mulberry fruit extract partially mitigates VPA-induced hepatocellular injury, primarily by enhancing glutathione-dependent antioxidant defenses.

Low-molecular-weight Ulva lacinulata extract exhibiting anti-inflammatory and pro-autophagic activities in RAW 264.7 macrophages: a promising candidate for the development of active ingredients targeting low-grade inflammation

The Polyphenol-Enriched Salix songarica Extract Alleviate High-Fat, High-Cholesterol Diet-Induced Inflammation via the LPC18:1/GPR120/β-Arrestin-2/NLRP3 Signaling Pathway

Salix songarica Andersson (S. songarica), a medicinal plant endemic to Xinjiang, exhibits high polyphenol content in its floral tissues. Although it shows anti-inflammatory potential, the underlying mechanisms remain unclear. This study investigated the therapeutic effects of polyphenol-enriched S. songarica flower extract (SSFP) on inflammation and dyslipidemia in high-fat, high-cholesterol diet (HFHCD)-fed ApoE−/− mice. SSFP administration significantly improved serum lipid profiles, hepatic function, and systemic inflammatory biomarkers in these mice, while also attenuating histopathological inflammation in the liver, kidney, and colon. Furthermore, SSFP treatment upregulated the expression of GPR120 and β-arrestin-2 and suppressed NLRP3 inflammasome activation. In vitro experiments further showed that the anti-inflammatory effect of LPC18:1 was consistent with SSFP. Together, our results demonstrate that SSFP alleviates inflammation through the LPC18:1/GPR120/β-arrestin-2/NLRP3 signaling axis, supporting its potential application as a natural functional food ingredient.

Antioxidant Activity of the Tithonia diversifolia, Moringa oleifera, and Curcuma longa Extract Combination Against Oxidative Stress in a Lipopolysaccharide-Induced Acute Lung Injury in Mice

The induction of acute inflammation in the lung tissue is triggered by lipopolysaccharide (LPS)-mediated activation of the TLR4 receptor. The combination of Tithonia diversifolia (T), Moringa oleifera (M), and Curcuma longa (C) extracts holds potential for synergistic anti-inflammatory and antioxidant effects. This study aimed to evaluate the effect of the aqueous TMC extract combination on reducing malondialdehyde (MDA) levels and enhancing Superoxide Dismutase (SOD) and Nuclear Factor Erythroid-2 Related Factor 2 (NRF2) expression in LPS-induced acute lung injury (ALI) in BALB/c mice. Thirty-six BALB/c mice were divided into five groups: negative control, LPS positive control, and three treatment groups receiving varying doses of the combined extract (TMC-1: 500/300/200; TMC-2: 200/500/300; TMC-3: 300/200/500 mg/kg BW). Treatments were administered orally for 14 days, followed by intraperitoneal LPS induction (0.5 mg/kg BW). Extract combination (TMC) significantly mitigated LPS-induced oxidative stress in a mouse acute lung injury model. Post-LPS therapy reduced MDA levels dose-dependently (16.96–8.68% vs. LPS 36.52%), restored SOD activity near normal (5.74–13.84% vs. LPS 25.23%), and normalized NRF2 expression (8.68–9.58% vs. LPS 17.11%). The TMC combination significantly reduced MDA levels and normalized the NRF2–SOD pathway, with the strongest SOD restoration at P2 (5.74%). These results confirm the role of TMC in strengthening the endogenous antioxidant system. This study provides scientific evidence for the development of the TMC extract combination as a potential phytopharmaceutical agent to mitigate oxidative stress and support tissue repair in inflammatory conditions such as ALI. Ultimately, this research supports UN SDG 3 (Targets 3.4 and 3.b) by developing an affordable respiratory protective agent, while simultaneously advancing SDG 15 through the sustainable pharmacological utilization of local plant biodiversity.