Bladder cancer is one of the most malignant tumors closely associated with macrophages. Polyporus polysaccharide (PPS) has shown excellent efficacy in treating bladder cancer with minimal side effects. However, the molecular mechanisms underlying the effects of PPS in inhibiting bladder cancer remain unclear. In this study, we used macrophages cultured alone or with T24 human bladder cancer cell culture supernatant as study models. We found that PPS enhanced the activities of IFN-γ-stimulated RAW 264.7 macrophages, as shown by the release of inducible nitric oxide synthase (INOS), secretion of tumor necrosis factor (TNF)-α and interleukin (IL)-6, phagocytosis activity, as well as expression of M1 phenotype indicators, such as CD40, CD284 and CD86. PPS acted upstream in activation cascade of nuclear factor (NF)-κB signaling pathways by interfering with IκB phosphorylation. In addition, PPS regulated NF-κB (P65) signaling by interfering with Toll-like receptor (TLR)-4, INOS and cyclooxygenase (COX)-2. Our results indicate that PPS activates macrophages through TLR4/NF-κB signaling pathways.
A linear regression method (LRG) had higher accuracy than an average method (AVG) and the concentration of the quantitative component was the major influencing parameter of the accuracy of the QAMS method.
Bladder cancer is one of the most malignant tumors closely associated with macrophage immune dysfunction. The Chinese medicine polyporus has shown excellent efficacy in treating bladder cancer, with minimal side effects. However, its material basis and mechanism of action remain unclear. A new water-soluble polysaccharide (HPP) with strong immunomodulatory activity was isolated from the fungus Polyporus umbellatus (Pers.) Fries. HPP had an average molecular weight of 6.88 kDa and was composed mainly of an <-(1→ 4)-linked D-galactan backbone. The immunomodulatory activity of HPP was determined in vitro, and the results revealed that it could obviously increase the secretion of immune factors by IFN-γ-stimulated macrophages, including nitric oxide (NO), interleukin-6 (IL-6), interleukin-1β (IL-1β), RANTES and interleukin-23 (IL-23), and the expression of the cell membrane molecule CD80. In addition, HPP was recognized by Toll-like receptor 2 (TLR2) and activated the signaling pathways of NF-κB and NLRP3 in a bladder cancer microenvironment model, indicating that HPP could enhance host immune system function. These findings demonstrated that HPP may be a potential immune modulator in the treatment of immunological diseases or bladder cancer therapy.
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