The aim of the present study was to investigate the role and mechanism of vascular cell adhesion molecule-1 (VCAM-1) in the development of rheumatoid arthritis (RA). One hundred and twenty patients with RA who had been admitted to the Huaihe Hospital of Henan University between January and December 2013 were enrolled in the study as the observation group, while, in the corresponding period, 30 healthy volunteers were enrolled as the control group. The serum levels of VCAM-1 and rheumatoid factor (RF) were detected using ELISA. The patients underwent conventional treatment and their serum VCAM-1 and RF levels were detected at different time-points to determine their correlation. The observation group exhibited significantly higher serum VCAM-1 and RF levels than the control group (P<0.01). Twenty-four hours after treatment, the serum VCAM-1 levels of the patients peaked (1,269.47±128.76 µg/l); 36 h after treatment, the serum RF levels peaked (34.42±8.45 U/ml); 1 month after treatment, the VCAM-1 and serum RF levels of the patients were lower than those prior to treatment (P<0.05). Pearson correlation analysis indicated that there was a significant, positive correlation between the serum VCAM-1 and RF levels in the patients with RA (r=0.852, P<0.01). In conclusion, the serum VCAM-1 levels of patients with RA increased and subsequently decreased as the condition was relieved, which could possibly be associated with the autoimmune and inflammatory reactions found in RA. Serum VCAM-1 levels can therefore reflect the disease condition and curative effects of treatment.

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Farrerol was found to possess neuroprotective effect; however, the mechanism remains unknown. The aim of the present study was to explore the effect of farrerol on MPP + -induced inflammation in mouse microglial BV-2 cells and to elaborate the underlying mechanism. MTT assay was performed to measure the cell viability. The pro-inflammatory mediators and cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α); inducible nitric oxide synthase; and cyclooxygenase 2 were measured. The expression of p-p65, p-IκBα, toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 were analyzed by western blot. We found that farrerol treatment improved cell viability in MPP + -induced BV-2 cells. MPP + -induced upregulation of IL-6, IL-1β, and TNF-α was inhibited by farrerol treatment. Farrerol treatment also attenuated MPP + -induced expression of inducible nitric oxide synthase and cyclooxygenase 2 as well as the activation of NF-κB in BV-2 cells. MPP + -induced TLR4 signaling was markedly diminished by farrerol treatment. Knockdown of TLR4 attenuated MPP + -induced inflammatory response in BV-2 cells. In conclusion, farrerol treatment attenuated MPP + -induced inflammatory response by inhibiting the TLR4 signaling pathway in BV-2 cells. The results indicated that farrerol could be used as a therapeutic agent for preventing or alleviating the neuroinflammation-related diseases, such as Parkinson's disease.

Long-term mobile phone use may increase the risk of developing glioma according to this meta-analysis.