ArticleEuropean journal of histochemistry : EJH2024
Astragaloside IV augments anti-PD-1 therapy to suppress tumor growth in lung cancer by remodeling the tumor microenvironment.
Article in European journal of histochemistry : EJH, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Effects of Kang'ai injection combined with chemotherapy on immune function in advanced non-small cell lung cancer: a meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Molecular mechanisms of astragaloside-IV in hepatocellular carcinoma therapy: a systematic review.BMC cancer · 2025Pooled it
- Astragaloside IV inhibits nasopharyngeal carcinoma progression by inhibiting SATB2/Wnt/PD-L1 pathway and enhancing the killing activity of T cells.European journal of histochemistry : EJH · 2026Article
- Astragaloside IV represses the immune evasion and acidic microenvironment of oral squamous cell carcinoma.Cellular & molecular biology letters · 2026Article
- Dynamic remodeling of the tumor immune microenvironment: immunometabolic regulatory networks of astragalus polysaccharides and astragaloside IV.Frontiers in pharmacology · 2026Review
- Mechanism of astragaloside A against lung adenocarcinoma based on network pharmacology combined with molecular dynamics simulation technique.Scientific reports · 2025Article
- Macrophage polarization in disease therapy: insights from astragaloside IV and cycloastragenol.Frontiers in pharmacology · 2025Review
- Astragaloside IV: a potential nemesis for gastric cancer.Frontiers in pharmacology · 2025Review
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6 authors.
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Abstract
Programmed cell death protein-1 (PD-1) inhibitors are increasingly utilized in the treatment of lung cancer (LC). Combination therapy has recently gained popularity in treating LC. This study aimed to assess the efficacy of combining Astragaloside IV (AS-IV) and anti-PD-1 in LC. C57BL/6J mice were subcutaneously injected with Lewis lung carcinoma (LLC) cells. After 3 weeks, the animals were sacrificed, and the tumors were harvested for analysis. Ki-67 immuno-labeling and TUNEL assay were used for evaluating cell proliferation and apoptosis in tumor tissues. In addition, anti-cleaved caspase 3 was used for immunolabelling of apoptotic cells. Immune cell infiltration (macrophages and T cells) and gene expression in tumor tissues were also investigated by using immunofluorescence staining. Compared to treatment with anti-PD-1 or AS-IV, the combination of AS-IV and anti-PD-1 notably reduced tumor volume and weight of LLC-bearing mice. Additionally, the combination treatment strongly induced the apoptosis and suppressed the proliferation in tumor tissues through inactivating PI3K/Akt and ERK signaling pathways, compared to single treatment group. Moreover, the combination treatment elevated levels of the M1 macrophage marker mCD86, reduced levels of the M2 macrophage marker mCD206, as well as upregulated levels of the T cell activation marker mCD69 in tumor tissues. Collectively, the combination treatment effectively inhibited tumor growth in LLC mice through promoting M1 macrophage polarization and T cell activation. These findings showed that combining AS-IV with anti-PD-1 therapy could be a promising therapeutic approach for LC.
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