Echinatin is an active ingredient in licorice, a traditional Chinese medicine used in the treatment of inflammatory disorders. However, the protective effect and underlying mechanism of echinatin against acute lung injury (ALI) is still unclear. Herein, we aimed to explore echinatin-mediated anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated ALI and its molecular mechanisms in macrophages. In vitro, echinatin markedly decreased the levels of nitric oxide (NO) and prostaglandin E2 (PGE₂) in LPS-stimulated murine MH-S alveolar macrophages and RAW264.7 macrophages by suppressing inducible nitric oxide synthase and cyclooxygenase-2 (COX-2) expression. Furthermore, echinatin reduced LPS-induced mRNA expression and release of interleukin-1β (IL-1β) and IL-6 in RAW264.7 cells. Western blotting and CETSA showed that echinatin repressed LPS-induced activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways through targeting transforming growth factor-beta-activated kinase 1 (TAK1). Furthermore, echinatin directly interacted with Kelch-like ECH-associated protein 1 (Keap1) and activated the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway to enhance heme oxygenase-1 (HO-1) expression. In vivo, echinatin ameliorated LPS-induced lung inflammatory injury, and reduced production of IL-1β and IL-6. These findings demonstrated that echinatin exerted anti-inflammatory effects in vitro and in vivo, via blocking the TAK1-MAPK/NF-κB pathway and activating the Keap1-Nrf2-HO-1 pathway.

Investigation on the chemical components of Valeriana jatamansi Jones (Caprifoliaceae), a new lignan with pyran-ring, dipsalignan G (1), along with eight known compounds (2–9) were isolated. Their structures were elucidated by extensive analysis of 1D, 2D NMR and HR-ESI-MS spectroscopic data. Additionally, possible biosynthetic pathway of 1 was proposed. Finally, biological evaluation results showed that 8 had significant scavenging ability to ABTS and DPPH free radicals, with IC₅₀ values of 1.35 ± 0.01 and 2.94 ± 0.01 μg/ml, respectively.

Background/Objectives: Toothpaste ingredients such as strontium chloride (SrCl₂) and potassium carbonate (K₂CO₃) are recognized for their desensitizing and remineralizing effects but may be absorbed through the oral mucosa. Their potential cytotoxic and cardiotoxic properties, however, remain inadequately characterized. Here, we investigated the effects of SrCl₂ and K₂CO₃ on mouse-induced pluripotent stem cells (iPSCs) and iPSC-derived cardiomyocytes (iPSC-CMs). Methods: Cells were exposed to varying concentrations of each compound for up to 72 h. Real-time cell analysis (xCELLigence RTCA Cardio system) was used to assess proliferation, and flow cytometry was used to evaluate cell viability. Functional properties of iPSC-CMs were examined using multi-electrode array (MEA) recordings and xCELLigence-based impedance measurements. Cardiac marker expression was examined via immunofluorescence and quantitative RT-PCR. Results: Both SrCl₂ and K₂CO₃ affected iPSC proliferation and reduced viability in a dose- and time-dependent manner, accompanied by altered embryoid body (EB) morphology and increased cell death. In iPSC-CMs, both compounds downregulated key cardiac genes and disrupted spontaneous beating activity, with effects intensifying at higher concentrations. Conclusions: These results demonstrate that SrCl₂ and K₂CO₃ induced dose-dependent cytotoxic and arrhythmogenic effects on iPSCs and iPSC-CMs. At elevated concentrations, these compounds impair iPSC-CM function and may pose safety concerns upon chronic exposure. Further mechanistic and long-term in vivo studies are warranted to assess their potential cardiotoxic risk in consumer oral care products.

Background/Objectives: Toothpaste ingredients such as strontium chloride (SrCl₂) and potassium carbonate (K₂CO₃) are recognized for their desensitizing and remineralizing ef-fects but may be absorbed through the oral mucosa. Their potential cytotoxic and cardio-toxic properties, however, remain inadequately characterized. Here, we investigated the effects of SrCl₂ and K₂CO₃ on mouse-induced pluripotent stem cells (iPSCs) and iPSC-derived cardiomyocytes (iPSC-CMs). Methods: Cells were exposed to varying con-centrations of each compound for up to 72 h. Real-time cell analysis (xCELLigence RTCA Cardio system) was used to assess proliferation, and flow cytometry was used to evaluate cell viability. Functional properties of iPSC-CMs were examined using multi-electrode ar-ray (MEA) recordings and the xCELLigence based impedance measurements. Cardiac marker expression was examined via immunofluorescence and quantitative RT-PCR. Results: Both SrCl₂ and K₂CO₃ affected iPSCs proliferation and reduced viability in a dose- and time-dependent manner, accompanied by altered embryoid body (EB) morphology and increased cell death. In iPSC-CMs, both compounds downregulated keys cardiac genes and disrupted spontaneous beating activity, with effects intensifying at the higher concentrations. Conclusions: These results demonstrate that SrCl₂ and K₂CO₃ induced dose-dependent cytotoxic and arrhythmogenic effects on iPSCs and iPSC-CMs. At elevated concentrations, these compounds impair iPSC-CMs function and may pose safety con-cerns upon chronic exposure. Further mechanistic and long-term in vivo studies are war-ranted to assess their potential cardiotoxic risk in consumer oral care products.