The antitumor and immunomodulatory activity of broken-spore of Ganoderma
lucidum polysaccharides (Gl-BSP) were investigated in vivo and in vitro. It was showed that Gl-BSP (50, 100, and 200 mg kg−1) exhibited antitumor effect against Sarcoma 180 (S180) in BALB/c mice. The Gl-BSP was not cytotoxicity in S180 cells and PG cells (human lung carcinoma cell) in vitro. However, serum from Gl-BSP-treated S180-bearing mice significantly inhibited S180 and PG cells proliferation in vitro. Moreover, Gl-BSP promoted the splenic lymphocyte proliferation induced by Con A or LPS, enhanced nature killer cell (NK cell) cytotoxic activity, augmented the percentage of neutral red phagocytosis by macrophages, and increased the percentage of the CD4+ or CD8+ subset in S180-bearing mice. The serum level of IFN-γ, TNF-α, and nitric oxide was increased by Gl-BSP. Gl-BSP also showed immunomodulatory activities in tumor-bearing mice. Furthermore, neutralization with anti-TNF-α and/or anti-IFN-γ significantly diminished growth inhibition induced by Gl-BSP-treated serum of S180-bearing mice in S180 or PG cells. These observations suggest that the antitumor activity of Gl-BSP may be mainly related to the activation of the immune response of the host organism by the stimulation of NK cells, T cells, and macrophages.
The aim of this study was to investigate the mechanism underlying the effects of Astragalus membranaceus injection (AMI) on myelopoiesis in myelosuppressed mice. At 72 h after cyclophosphamide injection (250 mg/kg), the mice were administered AMI (500 mg/kg) intraperitoneally for 6 consecutive days or an equivalent volume of saline as a control. Murine colony-forming unit-fibroblast (CFU-F) formation, production of IL-6 and GM-CSF by bone marrow stromal cells (BMSC), and bcl-2 protein and mRNA expression in BMSC were measured by CFU-F assay, ELISA, immunohistochemistry and in situ hybridization. The results indicated that AMI improved the hematopoietic microenvironment by enhancing the BMSC survival and proliferation of CFU-F, production of IL-6 as well as GM-CSF by BMSC and bcl-2 protein and mRNA expression in BMSC, which promoted myelopoiesis. The data may provide a mechanistic basis for applying this ancient Chinese herb to promote hematopoiesis as an efficacious adjuvant therapy against myelosuppression induced by anti-cancer therapy.
Aim: To study the effects (and the mechanisms thereof) of Ganoderma lucidum polysaccharides (Gl‐PS) on the proliferation and the anti‐tumor activity of cytokine‐induced killer (CIK) cells, and to make use of CIK cells as a means to investigate the interactions between Gl‐PS and cytokines.
Methods: CIK cells were prepared by using the standard protocol as a positive control. Experimental groups also underwent the standard protocol, except that Gl‐PS (400 mg/L or 100 mg/L) was added and the dose of anti‐CD3 and interleukin‐2 they received was reduced by 50% and 75%, respectively. For negative controls, Gl‐PS in the experimental protocol was replaced with soluble starch or methylcellulose (400 mg/L or 100 mg/L). CIK cell proliferation, cytotoxicity, and phenotype were determined by using the Trypan blue exclusion method, MTT assay, and flow cytometry.
Results: By synergizing cytokines, Gl‐PS (400 mg/L or 100 mg/L) could decrease the amount of cytokine in lymphokine activated killer (LAK) cells and CIK cells culture, but had no significant effect on the proliferation, cytotoxicity, or phenotype of LAK cells, or CIK cells induced by cytokines at higher doses alone, in which CIK cells expanded about 80‐fold and the main effectors, CD3+NK1.1+ cells, expanded by more than 15%. The cytotoxicity of CIK cells in experimental groups was 79.3%± 4.7%, 76.9%±6.8% versus the positive control 80.7%±6.8% against P815 (P>0. 05) and 88.9%±5.5%, 84.7%±7.9% versus the positive control 89.8%±4.5% against YAC‐1 (P>0. 05). The activity of Gl‐PS could mostly be blocked by anti‐CR3.
Conclusion: Gl‐PS was shown to be a promising biological response modifier and immune potentiator. The effect of Gl‐PS on CIK cells is possibly mediated primarily through complement receptor type 3.
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