{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T13:19:10Z","timestamp":1787750350251,"version":"build-2784847793"},"reference-count":46,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>Abstract:<\/jats:title>\n                  <jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Hepatocellular carcinoma (HCC) is an aggressive malignancy with frequent recurrence and strong immune evasion. Programmed death ligand-1 (PD-L1) facilitates immune evasion by suppressing T-cell activity. Andrographolide (AD), a natural diterpenoid with anti-inflammatory, antiviral, and immunomodulatory properties, has demonstrated antitumor potential.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>MATERIALS AND METHODS:<\/jats:title>\n                    <jats:p>Subcutaneous HCC mouse models assessed the antitumor and immune-activating effects of AD. CCK-8 assay, colony-formation assay, apoptosis analyses, and western blot investigated AD\u2019s impacts on Huh-7 cell proliferation, apoptosis, and cell cycle. Immunofluorescence staining and flow cytometry collectively measured PD-L1 expression after AD treatment. Molecular docking and cellular thermal shift assay detected the targeted binding between AD and STAT3. Finally, recombinant interleukin-6 (rIL-6), a STAT3 activator, was used to verify whether AD-mediated effects on Huh-7 cell viability and PD-L1 expression were STAT3-dependent.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n                      , AD significantly inhibited mouse tumor growth, decreased PD-L1 expression in tumor tissues, and enhanced T-cell infiltration.\n                      <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                      , through cell experiments, AD bound to STAT3 and inhibited tumor cell proliferation, induced apoptosis, and downregulated PD-L1 protein levels by suppressing the phosphorylation of STAT3. Treatment with rIL-6 significantly reversed AD\u2019s antitumor effects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSION:<\/jats:title>\n                    <jats:p>AD inhibits HCC progression and PD-L1 expression by blocking STAT3 phosphorylation, providing a theoretical foundation for developing AD-based therapeutic strategies against HCC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/ijp.ijp_860_25","type":"journal-article","created":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T18:00:26Z","timestamp":1782410426000},"page":"391-400","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Andrographolide inhibits hepatocellular carcinoma progression and programmed death ligand-1 expression by blocking STAT3 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