Scutellarin has a good myocardial protective effect. However, the underlying mechanism of scutellarin on cardiomyocyte pyroptosis remains unclear. In this study, we elucidated the mechanism of scutellarin to protect the injured myocardium. The molecular docking technique was used to predict the targets of scutellarin in protecting against myocardial injury. H9c2 cell pyroptosis was induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Then, the activities of CK and LDH were measured through a colourimetric assay. The level of cTnI was quantified by ELISA. mRNA expressions of NLRP3, cysteine-dependent aspartate-specific protease-1 (caspase-1), gasdermin D (GSDMD), interleukin-1β (IL-1β), and interleukin-18 (IL-18) were analyzed using RT-qPCR. Protein expressions of NLRP3, caspase-1, and GSDMD were detected by the immunofluorescence technique. Protein expression of NLRP3 was analysed by using Western blotting. Scutellarin had a good binding affinity with NLRP3, caspase-1, and GSDMD. Compared with LSP and ATP-treated cells, concentrations of 25, 50, and 100 µmol L⁻¹ scutellarin reduced CK and LDH activities and the level of cTnI, decreased the mRNA expression of NLRP3, caspase-1, and GSDMD. In the mechanism study, scutellarin decreased mRNA expressions of NLRP3, caspase-1, GSDMD, IL-1β, and IL-18, and reduced the fluorescence expressions of NLRP3, caspase-1, and GSDMD. Scutellarin reduced the protein expression of NLRP3. Scutellarin inhibits myocardial cell pyroptosis induced by LPS and ATP, and the mechanism is related to the NLRP3/caspase-1/GSDMD signalling pathway.

The flowers of Panax ginseng C. A. Mey. (PG) and Panax notoginseng (Burkill) F. H. Chen ex C. H. Chow (PN) are morphologically indistinguishable after drying, leading to prevalent adulteration that compromises product quality and consumer safety. To address this issue, we developed a rapid, closed-tube molecular authentication method based on high-resolution melting (HRM) analysis. Species-specific primer pairs were designed to target the conserved ITS and rbcL-accD regions, with PNG-2 selected as the optimal candidate owing to its stable genotyping performance and moderate GC content. Our results established GC content, rather than amplicon length, as the primary determinant of the melting temperature (Tm). Notably, the experimentally measured Tm values were consistently 0.7–1.5 °C higher than theoretical predictions, a discrepancy attributable to the stabilizing effect of the saturated fluorescent dye. To ensure maximum diagnostic reliability, the HRM results were cross-validated through a three-tier system comprising ITS2 phylogenetic analysis, agarose gel electrophoresis, and Sanger sequencing. The practical utility and matrix robustness of the assay were further verified using a diversified validation cohort of 30 commercial samples, including 24 floral batches and 6 root-derived products (root slices and ultramicro powders). The HRM profiles demonstrated 100% concordance with DNA barcoding results, effectively identifying mislabeled products across different botanical matrices and processing forms. This methodology, which can be completed within 3 h, provides a significantly more cost-effective and rapid alternative to traditional sequencing-based methods for large-scale market surveillance and industrial quality control.

Alcoholic liver disease (ALD) is a condition caused by alcohol abuse. Although its incidence is rapidly increasing, effective treatments for this disease remain limited. The pathogenesis of ALD involves multiple aspects, such as direct damage from alcohol, oxidative stress, inflammation, lipid metabolism disorders, and dysbiosis of the gut microbiota. Under the combined action of multiple damaging factors, liver inflammation worsens and leads to liver fibrosis. In this review, we focused on in vitro and in vivo experiments to investigate the mechanistic pathways by which natural products exert effects against the progression of ALD. The accumulated and collected data indicate that some natural products may regulate oxidative stress, inflammation, autophagy, lipid metabolism, and the intestinal barrier, thereby protecting the liver. This review presents an updated overview of the potential benefits of these natural products for the prevention and treatment of ALD, identifying potential new therapeutic lead compounds and providing a reference for innovative drug development and clinical treatment for ALD.