Ganoderma lucidum polysaccharides promote T lymphocyte infiltration into tumor by regulating expression of ICAM-1 in endothelial cells.
10.19540/j.cnki.cjcmm.20210726.401
- Author:
Xiao-Yan XU
1
;
Xia LUO
1
;
Yi SONG
1
;
Zhou ZHOU
1
;
Fang LI
1
;
Meng-Yao YU
1
Author Information
1. Sichuan Academy of Chinese Medical Sciences Chengdu 610041, China Sichuan Provincial Key Laboratory of Medicinal Materials Quality and Drug Discovery in Traditional Chinese Medicine Chengdu 610041, China Laboratory for Systematic Research and Development of Fungus Medicinal Materials Chengdu 610041, China.
- Publication Type:Journal Article
- Keywords:
Ganoderma lucidum polysaccharides;
ICAM-1;
T lymphocyte;
endothelial cell;
tumor
- MeSH:
Animals;
Endothelial Cells/metabolism*;
Intercellular Adhesion Molecule-1/genetics*;
Mice;
NF-kappa B/metabolism*;
Neoplasms;
Polysaccharides;
Reishi;
Signal Transduction;
T-Lymphocytes;
Tumor Necrosis Factor-alpha
- From:
China Journal of Chinese Materia Medica
2021;46(19):5072-5079
- CountryChina
- Language:Chinese
-
Abstract:
Polysaccharide is among the main active components of Ganoderma lucidum for tumor prevention and treatment. Howe-ver, it remains unclear whether it has synergy with tumor immunotherapy. This study evaluated the effect of G. lucidum polysaccharides(GLP) on the infiltration of T lymphocytes into tumor and the underlying mechanism, in order to provide a reference for its application in tumor immunotherapy. GLP were prepared by water extraction and alcohol precipitation combined with Sevag method and then given(intraperitoneal injection) to the mice bearing B16-F10 cells at 25, 50 and 100 mg kg~(-1), respectively, to evaluate the effect on tumor growth. The infiltration of CD3~+ and CD8~+ T cells and the expression of intercellular cell adhesion molecule-1(ICAM-1) in tumor were detected by immunohistochemistry. EA.hy926 cells were treated with 50, 100 and 200 μg·mL~(-1) GLP, and the expression of ICAM-1 was determined by Western blot. The adhesion of EA.hy926 cells treated with GLP was measured with fluorescence-labeled Jurkat cells. To analyze the mechanism based on NF-κB pathway, this study determined the protein levels of nuclear factor kappa-B(NF-κB) p65, alpha inhibitor of NF-κB(IκBα), p-NF-κB p65 and p-IκBα by Western blot. The results showed that GLP can significantly inhibit the tumor growth in mice bearing B16-F10 cells, promote the infiltration of CD3~+ and CD8~+ T cells in tumor, and increase the expression of ICAM-1 in tumor. Meanwhile, GLP could also enhance the expression of ICAM-1 in EA.hy926 cells, thus strengthen the adhesion to Jurkat cells, induce phosphorylation and protein degradation of IκBα, and raise the expression and phosphorylation level of NF-κB p65. These results suggested that GLP could promote the expression of ICAM-1 through NF-κB pathway and further enhance the infiltration of T lymphocytes into tumor, thereby inhibiting tumor growth. This study lays a foundation for the further application of GLP in tumor immunotherapy.
