Total flavonoids extracted from

Background: Flavonoids are primary bioactive components of Methods: A nude mouse model of subcutaneous tumor formation of hepatocellular carcinoma was established. Following PCPTF treatment, the pathological changes, tumor cell proliferation and apoptosis, serum inflammatory factors and oxidative stress levels, and the levels of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) proteins in tumor tissues were detected. Lipopolysaccharides (LPS) was applied to construct liver cancer cell inflammation models in vitro. After treatment of PCPTF and JAK2 agonist coumermycin A1 (CA1) in the cells, protein levels, cell proliferation, inflammation, and oxidative stress were evaluated to explore the mechanism of PCPTF in improving liver cancer. Results: In mice with liver cancer, PCPTF treatment inhibited tumor growth, improved the pathological changes, down-regulated interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), reactive oxygen species (ROS), up-regulated superoxide dismutase (SOD), and suppressed JAK2 and STAT3 phosphorylation. In liver cancer cells, PCPTF blocked the JAK2/STAT3 pathway, proliferation, and the release of inflammatory factors, regulated oxidative stress, and promoted apoptosis. However, CA1 reversed the effect of PCPTF on liver cancer cells. Conclusions: PCPTF suppresses the progression of liver cancer by ameliorating oxidative stress and inflammatory response, primarily through the regulation of the JAK2/STAT3 signaling pathway.