Tumor necrosis factor-α-induced protein 8-like-2 is involved in the activation of macrophages by Astragalus polysaccharides in vitro.

In previous years, studies have shown that Astragalus polysaccharides (APS) can improve cellular immunity and humoral immune function, which has become a focus of investigations. Tumor necrosis factor­α­induced protein 8­like 2 (TIPE2) is a negative regulator of immune reactions. However, the effect and underlying mechanisms of TIPE2 on the APS­induced immune response remains to be fully elucidated. The present study aimed to examine the role of TIPE2 and its underlying mechanisms in the APS­induced immune response. The production of nitric oxide (NO) was detected in macrophages in vitro following APS stimulation. In addition, the present study interfered with the expression of TIPE2 in macrophages, and examined the production of cytokines, NO and components of the mitogen­activate protein kinase (MAPK) signaling pathway following APS stimulation. The results showed that APS was able to activate macrophages by inducing the production of interleukin (IL)­1ß, tumor necrosis factor (TNF)­α, IL­6 and NO. Furthermore, RAW264.7 cells were stimulated with APS when TIPE2 was silenced, and it was found that the production of TNF­α, IL­6, IL­1ß and NO were upregulated, and the signaling pathway of MAPK was activated. Taken together, these results demonstrated that TIPE2 had an important negative effect on the APS­induced production of inflammatory cytokines and NO via the MAPK signaling pathway.

Inhibitory effects of oligochitosan on TNF-α, IL-1ß and nitric oxide production in lipopolysaccharide-induced RAW264.7 cells.

Oligochitosan has been reported to possess anti-inflammatory properties; however, the mechanism of the antiinflammatory effects of oligochitosan remains unknown. The present study aimed to investigate the expression levels of inflammatory cytokines and the production of nitric oxide (NO), in the nuclear factor (NF)-κB pathway of lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. The results of the present study demonstrated that different concentrations of oligochitosan could significantly lower the levels of NO, tumor necrosis factor (TNF)-α and interleukin (IL)-1ß, released from LPS-stimulated RAW264.7 cells. This was shown to be mediated through inhibiting the activation of the NF-κB pathway. These results demonstrate that oligochitosan may efficiently inhibit inflammation and has the potential to be an effective anti-inflammatory agent.

Cyclin D1 G870A polymorphism and risk of nasopharyngeal carcinoma: a meta-analysis.

Recently, there have been a number of studies on the association between cyclin D1 G870A polymorphism and nasopharyngeal carcinoma risk. However, the results of previous reports remain controversial and ambiguous. Thus, we performed a meta-analysis to explore more precisely the association between cyclin D1 G870A polymorphism and the risk of nasopharyngeal carcinoma. No significant association was found between cyclin D1 G870A polymorphism and nasopharyngeal carcinoma risk in total population analysis. In the subgroup meta-analysis by ethnicity, a negative association was shown in Caucasian subgroup, and no significant association in any genetic models among Asians was observed. In summary, positive results have been shown on the search for polymorphic variants influencing the risk of NPC. This meta-analysis provides evidence of the association between CCND1 G870A polymorphism and NPC risk, supporting the hypothesis that CCND1 870A allele probably acts as an important NPC protective factor in Caucasians but not in Asians. Since the results of our meta-analysis are preliminary and may be biased by the relatively small number of subjects, they still need to be validated by well-designed studies using larger samples in the future.

Lycium barbarum polysaccharides induce Toll-like receptor 2- and 4-mediated phenotypic and functional maturation of murine dendritic cells via activation of NF-κB.

Dendritic cells (DCs) are potent antigen­presenting cells that play pivotal roles in the initiation of primary immune responses. Lycium barbarum polysaccharides (LBPs) are known to have a variety of immunomodulatory functions. However, the cellular and molecular mechanisms underlying their therapeutic effects are poorly understood. In this study, we report that LBPs induce phenotypic and functional maturation of DCs. LBPs upregulated DC expression of I­A/I­E and CD11c, enhanced DC allostimulatory activity and induced IL­12p40 production. Furthermore, the activity of LBPs on DCs was significantly reduced by treating the cells with anti­TLR2 or anti­TLR4 antibody prior to LBPs, indicating that both are possible receptors of LBPs. Maturation of DCs by LBPs was able to directly activate the nuclear transcription factor NF­κB p65. The results revealed that LBP stimulation induces the phenotypic and functional maturation of DCs via TLR2- and/or TLR4-mediated NF­κB signaling pathways.

[Detection of the serum level of interleukin-17 and interleukin-6 in the chronic hepatitis B patients].

OBJECTIVE: To research serum level of interleukin-17 (IL-17) associated with the progression of hepatic injury in the chronic patients with hepatitis B. METHODS: The serum level of IL-17 was measured by ELISA and the serum levels of IL-6, IL-8 were measured by RIA in patient groups and healthy group, the patient groups including 42 mild patients, 37 moderate patients and 38 severe patients. RESULTS: IL-17,IL-6 and IL-8 levels in patient patients were significantly higher than those in healthy people (P < 0.01). There is no significant difference among mild patients and moderate patients. Compared with mild patients and moderate patients,the cytokines lever were significantly higher in severe patients (P < 0.01). CONCLUSION: IL-17 as a new cytokine probably play a multiple role as immune factor and inflammation element in the progression of the chronic hepatitis B disease. Maybe, it can provide a new approach to the therapy of the chronic hepatitis B.

Evaluation of plasma urokinase-type plasminogen activator and urokinase-type plasminogen-activator receptor in patients with acute and chronic hepatitis B.

INTRODUCTION: Urokinase-type plasminogen activator (uPA) and urokinase-type plasminogen activator receptor (uPAR) are known to be important factors in the pathogenesis of tumors and certain non-viral inflammatory diseases. However, their role in infectious virus diseases such as hepatitis B has been less well studied. This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the inflammatory damage to liver cells caused by the hepatitis B virus. We therefore analyzed their role and clinicopathological significance in patients with acute or chronic hepatitis B. MATERIALS AND METHODS: Eighty patients with acute or chronic hepatitis B, together with 30 healthy controls, were enrolled. uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay (ELISA) kits. RESULTS: The levels of uPA and uPAR in patients with acute or chronic hepatitis B significantly exceeded those in healthy controls (p<0.05). Patients with severe chronic hepatitis B had significantly higher levels of uPA and uPAR than those with moderate and mild chronic disease (p<0.05) and those with acute hepatitis B (p<0.05). Moreover, the plasma uPA and uPAR markedly increased in the acute stage (p<0.05) and dramatically decreased in the remission stage (p<0.05), but in all stages levels exceeded those in healthy subjects (p<0.05). In addition, the concentration of plasma uPAR was positively correlated with prothrombin (PT) (r=0.605, p<0.01) and total bilirubin (TBIL) (r=0.649, p<0.01). CONCLUSIONS: It is suggested that the plasma levels of uPA and uPAR are closely related to the degree and period of inflammation in patients with acute or chronic hepatitis B, and that uPA and uPAR might be important indicators for disease progression.