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Safflower Yellow Inhibits Progression of Hepatocellular Carcinoma by Modulating Immunological Tolerance via FAK Pathway.
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- Author(s): Ji, Hua-feng; Yang, Zi-qiang; Han, Jun-jun; Li, He-fang; Jin, Zhao-qing; Chen, Wei-qing; Chen, Fei-hua; Gong, Mou-chun
- Source:
Chinese Journal of Integrative Medicine; Apr2024, Vol. 30 Issue 4, p339-347, 9p- Subject Terms:
THERAPEUTIC use of antineoplastic agents; CHINESE medicine; IMMUNOLOGICAL tolerance; IN vitro studies; FLOW cytometry; CHEMOKINES; BIOLOGICAL models; T cells; PROGRAMMED death-ligand 1; IMMUNOGLOBULINS; ENZYME-linked immunosorbent assay; CELLULAR signal transduction; PLANT extracts; LUMINESCENCE spectroscopy; GENE expression; MICE; WESTERN immunoblotting; ANIMAL experimentation; CYTOKINES; HEPATOCELLULAR carcinoma; DISEASE progression - Source:
- Additional Information
- Abstract: Objective: To explore the anti-tumor effect of safflower yellow (SY) against hepatocellular carcinoma (HCC) and the underlying potential mechanism. Methods: An in vitro model was established by mixing Luc-Hepa1-6 cells and CD3+CD8+ T cells, followed by adding programmed cell death protein 1 (PD-1) antibody (Anti-mPD-1) with or without SY. The apoptosis was detected by flow cytometry and the level of inflammatory cytokines was determined by enzyme-linked immunosorbent assay. The protein levels of programmed cell death 1 ligand 1 (PD-L1), chemokine ligand (CCL5), C-X-C motif chemokine ligand 10 (CXCL10) were measured by Western blot. An in situ animal model was established in mice followed by treatment with anti-mPD-1 with or without SY. Bioluminescence imaging was monitored with an AniView 100 imaging system. To establish the FAK-overexpressed Luc-Hepa1-6 cells, cells were transfected with adenovirus containing pcDNA3.1-FAK for 48 h. Results: The fluorescence intensity, apoptotic rate, release of inflammatory cytokines, and CCL5/CXCL10 secretion were dramatically facilitated by anti-mPD-1 (P<0.01), accompanied by an inactivation of PD-1/PD-L1 axis, which were extremely further enhanced by SY (P<0.05 or P<0.01). Increased fluorescence intensity, elevated percentage of CD3+CD8+ T cells, facilitated release of inflammatory cytokines, inactivated PD-1/PD-L1 axis, and increased CCL5/CXCL10 secretion were observed in Anti-mPD-1 treated mice (P<0.01), which were markedly enhanced by SY (P<0.05 or P<0.01). Furthermore, the enhanced effects of SY on inhibiting tumor cell growth, facilitating apoptosis and inflammatory cytokine releasing, suppressing the PD-1/PD-L1 axis, and inducing the CCL5/CXCL10 secretion in Anti-mPD-1 treated mixture of Luc-Hepa1-6 cells and CD3+CD8+ T cells were abolished by FAK overexpression (P<0.01). Conclusion: SY inhibited the progression of HCC by mediating immunological tolerance through inhibiting FAK. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Chinese Journal of Integrative Medicine is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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