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Pyroptosis, a form of cell death associated with inflammation, is known to be involved in diabetic nephropathy (DN), and discoid domain receptor 1 (DDR1), an inflammatory regulatory protein, is reported to be associated with diabetes. However, the mechanism underlying DDR1 regulation and pyroptosis in DN remains unknown. We aimed to investigate the effect of DDR1 on renal tubular epithelial cell pyroptosis and the mechanism underlying DN. In this study, we used high glucose (HG)-treated HK-2 cells and rats with a single intraperitoneal injection of streptozotocin as DN models. Subsequently, the expression of pyroptosis-related proteins (cleaved caspase-1, GSDMD-N, Interleukin-1β [IL-1β], and interleukin-18 [IL-18]), DDR1, phosphorylated NF-κB (p-NF-κB), and NLR family pyrin domain-containing 3 (NLRP3) inflammasomes were determined through Western blotting. IL-1β and IL-18 levels were determined using ELISA. The rate of pyroptosis was assessed by propidium iodide (PI) staining. The results revealed upregulated expression of pyroptosis-related proteins and increased concentration of IL-1β and IL-18, accompanied by DDR1, p-NF-κB, and NLRP3 upregulation in DN rat kidney tissues and HG-treated HK-2 cells. Moreover, DDR1 knockdown in the background of HG treatment resulted in inhibited expression of pyroptosis-related proteins and attenuation of IL-1β and IL-18 production and PI-positive cell frequency

This paper proposes a novel narrowband interference suppression algorithm used in the direct sequence spread spectrum system. The proposed algorithm locates interference and forms the notch band based on the spectrum after noncoherent accumulation, which can reduce the impacts of noise on interference detection. Simulation results show that the proposed algorithm can locate interference accurately and have a better bit error rate performance than conventional algorithms, especially when the interference power is close to the anti-interference tolerance of the system.

Currently, selenium and polysaccharide combinations can be identified as three forms: natural selenium polysaccharides, synthetic selenium polysaccharides and selenium nanoparticles decorated with polysaccharides. Previous studies have indicated that these three combinations generally show better bioactivities, including immunomodulation, anti-tumour, antioxidation and glucose regulation, than those of either selenium or polysaccharides alone. Although they have not yet been developed as new drugs for clinical trials, results from previous studies have already shown their therapeutic potential for the future. In this article, we summarize our current state of understanding of the sources, preparation methods, physicochemical characteristics and bioactivities of these combinations for the discovery of novel therapeutic drugs and adjuvants.

The aim of this study was to examine the effect of extracellular polysaccharide (PEP) from Antarctic bacterium Pseudoaltermonas sp. S-5 on RAW 264.7 cells together with the underlying signaling pathways. Our results illustrated that PEP induced dendritic-like morphological change in RAW 264.7 cells, and increased the productions of nitric oxide (NO) and tumor necrosis factor-α (TNF-α). PEP could also enhance phagocytic activity of RAW 264.7 cells. Results of immunofluorescence staining and immunoblotting indicated that PEP caused the nuclear translocation of nuclear factor (NF)-κB subunit p65, the degradation of IκB-α and up-expression of phosphorylated p38 mitogen-activated protein kinase (MAPK) in RAW 264.7 cells. According to pharmacological evaluation with specific enzyme inhibitors, both NF-κB and p38 MAPK signaling pathways were involved in the generation of NO and TNF-α induced by PEP. All these results indicated that PEP from Antarctic bacterium Pseudoaltermonas sp. S-5 activated RAW 264.7 cells through NF-κB and p38 MAPK signaling pathways.

Dendritic cells (DCs) are the key regulators of immune responses. In this study, the effect of an exopolysaccharide (EPS) from the culture broth of Trichoderma pseudokoningii on the phenotypic and functional maturation of murine DCs and its underlying molecular mechanisms were investigated. It showed that EPS induced the morphological changes of DCs and the enhanced expression of DCs featured surface molecules CD11c, CD86, CD80 and major histocompatibility complex II (MHC-II). Flow cytometry analysis showed that the treatment with EPS could reduce FITC-dextran uptake by DCs. Sequentially, the results of ELISA indicated that EPS could increase the production of interleukin-12p70 (IL-12p70) in culture supernatant of DCs. Immunofluorescence staining and western blot analysis further revealed that EPS significantly prompted nuclear factor (NF)-κB subunit p65 translocation, IκB-α protein degradation, and p38 mitogen-activated protein kinase (MAPK) phosphorylation. And the production of IL-12p70 was significantly decreased in condition of the inhibition of p38 or NF-κB signaling pathway. These findings suggested that EPS could induce DCs maturation through both p38 MAPK and NF-κB signaling pathways.