{
  "abstract": "Previous studies have reported that the combination of Astragali Radix and Angelicae Sinensis Radix (AR-ASR) can ameliorate atherosclerosis (AS) through anti-inflammatory effects; however, the exact mechanistic underpinnings still await further clarification. The present study investigates the anti-atherosclerotic action of AR-ASR from the perspective of PANoptosis (encompassing apoptosis, pyroptosis, and necroptosis). To ascertain the chief active ingredients of the AR plus ASR mixture, UPLC-MS/MS detection was utilized. To predict potential therapeutic targets, a multi-faceted bioinformatics strategy was applied, integrating transcriptomics, single-cell sequencing, network pharmacology, molecular docking, and molecular dynamics simulations. In vivo, male ApoE-deficient mice were allocated at random into the model cohort, AR-ASR low-, medium-, and high-dose groups (AR-ASR L, AR-ASR M, and AR-ASR H, respectively), atorvastatin group (ATV), and control group (age-matched wild-type C57BL/6J mice). Atherosclerosis was induced by 12 weeks of high-fat diet feeding, followed by 4 weeks of oral gavage treatment. Assessment parameters included aortic intimal hyperplasia thickness, serum lipid levels, vascular inflammatory factor expression, endothelial function, and the gene and protein expression levels of PANoptosis- and p38MAPK/p53 signaling pathway-related molecules. For in vitro experiments, POVPC-stimulated AVECs were used as an oxidative damage model and then treated with AR-ASR-containing serum. Cell proliferation activity, cell injury rate, and the expression levels of PANoptosis markers and p38MAPK/p53 signaling pathway-related molecules were measured. Furthermore, in the presence of a p38MAPK agonist, the protective effect of AR-ASR on AVECs and its underlying mechanism were investigated. Bioinformatics analysis suggested that AR-ASR modulates PANoptosis and interferes with AS via the p38MAPK/p53 signaling axis. In vivo, AR-ASR treatment reduced serum lipid levels, attenuated aortic intimal hyperplasia, decreased plasma inflammatory cytokine levels and vascular inflammatory factor expression, improved endothelial function, and suppressed both vascular PANoptosis and p38MAPK/p53 pathway activation. In vitro, POVPC induced oxidative damage and PANoptosis in AVECs. AR-ASR-containing serum promoted AVEC viability, reduced LDH release, inhibited the expression of PANoptosis-related markers, and downregulated p38MAPK/p53 signaling pathway protein expression. Furthermore, in the presence of a p38MAPK agonist, the inhibitory effects of AR-ASR on cellular PANoptosis and p38MAPK/p53 pathway activation were significantly attenuated. The AR-ASR compatibility suppresses p38MAPK/p53 pathway activation, thereby inhibiting vascular endothelial PANoptosis-driven inflammatory responses and ameliorating atherosclerotic vascular pathology.",
  "abstract_shown": true,
  "affiliations": [
    "Key Laboratory of Hunan Provincial for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Hunan 410208, China"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 11,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Wanyu Li"
    },
    {
      "affs": [
        0
      ],
      "name": "Qingyin Long"
    },
    {
      "affs": [
        0
      ],
      "name": "Xinying Fu"
    },
    {
      "affs": [
        0
      ],
      "name": "Yanling Li"
    },
    {
      "affs": [
        0
      ],
      "name": "Lu Ma"
    },
    {
      "affs": [
        0
      ],
      "name": "Wei Tan"
    },
    {
      "affs": [
        0
      ],
      "name": "Zhongji Hu"
    },
    {
      "affs": [
        0
      ],
      "name": "Yanyan Zhang"
    },
    {
      "affs": [
        0
      ],
      "name": "Yan She"
    },
    {
      "affs": [
        0
      ],
      "name": "Wei Zhang",
      "orcid": "0000-0002-2161-7355"
    },
    {
      "affs": [
        0
      ],
      "name": "Changqing Deng"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/btq0bnhxzhmm3.bib",
  "cited_by": 0,
  "doi": "10.3390/ijms27188330",
  "fulltext_url": null,
  "id": "btq0bnhxzhmm3",
  "issns": [
    "1422-0067"
  ],
  "landing_url": "https://www.mdpi.com/1422-0067/27/18/8330",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2403|Atherosclerosis and Cardiovascular Diseases"
    ]
  ],
  "openalex": "W7214492754",
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-19",
  "publisher": "MDPI AG",
  "ris": "https://research.draconitic.com/paper/btq0bnhxzhmm3.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:18:55Z",
      "native_id": "10.3390/ijms27188330",
      "source": "crossref",
      "url": "https://www.mdpi.com/1422-0067/27/18/8330"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "openalex:2403|Atherosclerosis and Cardiovascular Diseases",
      "subfield": "immunology"
    }
  ],
  "title": "The Compatibility of Astragali Radix and Angelicae Sinensis Radix Attenuates Atherosclerosis by Suppressing Vascular Endothelial PANoptosis via the p38 MAPK/p53 Pathway: A Multi-Omics and Experimental Study",
  "title_text": "The Compatibility of Astragali Radix and Angelicae Sinensis Radix Attenuates Atherosclerosis by Suppressing Vascular Endothelial PANoptosis via the p38 MAPK/p53 Pathway: A Multi-Omics and Experimental Study",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:18:55Z",
  "url": "https://research.draconitic.com/paper/btq0bnhxzhmm3",
  "venue": "International Journal of Molecular Sciences",
  "versions": []
}