Inhibitory effects of silver nanoparticles on H1N1 influenza A virus in vitro.

Silver nanoparticles have demonstrated efficient inhibitory activities against human immunodeficiency virus (HIV) and hepatitis B virus (HBV). However, the effects of silver nanoparticles against H1N1 influenza A virus remain unexplored. In this study, the interaction of silver nanoparticles with H1N1 influenza A virus was investigated. Silver nanoparticles with mean particle diameters of 10nm were prepared for the hemagglutination inhibition test, the embryo inoculation assay, and the Mosmann-based 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, where these tests were used to determine the inhibitory activity of silver nanoparticles on H1N1 influenza A virus. MDCK cells were used as the infection model. Electron microscopy analysis and flow cytometry assay were used to determine whether silver nanoparticles could reduce H1N1 influenza A virus-induced apoptosis in MDCK cells. This study demonstrates that silver nanoparticles have anti-H1N1 influenza A virus activities. The inhibitory effects of silver nanoparticles on influenza A virus may be a novel clinical strategy for the prevention of influenza virus infection during the early dissemination stage of the virus.

Nicotinamide overload may play a role in the development of type 2 diabetes.

AIM: To investigate whether nicotinamide overload plays a role in type 2 diabetes. METHODS: Nicotinamide metabolic patterns of 14 diabetic and 14 non-diabetic subjects were compared using HPLC. Cumulative effects of nicotinamide and N(1)-methylnicotinamide on glucose metabolism, plasma H(2)O(2) levels and tissue nicotinamide adenine dinucleotide (NAD) contents of adult Sprague-Dawley rats were observed. The role of human sweat glands and rat skin in nicotinamide metabolism was investigated using sauna and burn injury, respectively. RESULTS: Diabetic subjects had significantly higher plasma N(1)-methylnicotinamide levels 5 h after a 100-mg nicotinamide load than the non-diabetic subjects (0.89 +/- 0.13 micromol/L vs 0.6 +/- 0.13 micromol/L, P < 0.001). Cumulative doses of nicotinamide (2 g/kg) significantly increased rat plasma N(1)-methylnicotinamide concentrations associated with severe insulin resistance, which was mimicked by N(1)-methylnicotinamide. Moreover, cumulative exposure to N(1)-methylnicotinamide (2 g/kg) markedly reduced rat muscle and liver NAD contents and erythrocyte NAD/NADH ratio, and increased plasma H(2)O(2) levels. Decrease in NAD/NADH ratio and increase in H(2)O(2) generation were also observed in human erythrocytes after exposure to N(1)-methylnicotinamide in vitro. Sweating eliminated excessive nicotinamide (5.3-fold increase in sweat nicotinamide concentration 1 h after a 100-mg nicotinamide load). Skin damage or aldehyde oxidase inhibition with tamoxifen or olanzapine, both being notorious for impairing glucose tolerance, delayed N(1)-methylnicotinamide clearance. CONCLUSION: These findings suggest that nicotinamide overload, which induced an increase in plasma N(1)-methylnicotinamide, associated with oxidative stress and insulin resistance, plays a role in type 2 diabetes.

Complete Freund's adjuvant promotes the increases of IFN-gamma and nitric oxide in suppressing chronic arthritis induced by pristane.

The aim of this study was to determine therapeutic effects of complete Freund's adjuvant (CFA) on the progression and relapsing of pristine-induced arthritis (PIA) and investigate the mechanism involved. Chronic relapsing arthritis was induced by pristine in LEW rats. After onset of arthritis, rats were intradermally injected CFA and rats in control group were injected the same volume of PBS. Arthritis was monitored visually, and joint pathology was examined histologically. Cytokine mRNA expression in inguinal lymph nodes was assessed by RT-PCR. The levels of nitric oxide (NO) in serum were measured by colorimetric assay. The results showed that CFA significantly suppressed the progression and relapsing of PIA. Relapsing rate of PIA in CFA-treated group was 12.5% and it was 85.7% in PBS-control group (P < 0.005). CFA markedly inhibited the infiltration of inflammatory cells and cartilage damage in the joints of CFA-treated rats and promoted the increases of IFN-y mRNA and NO levels. The present study provided an implication that adjuvant therapy may be a new strategy for the treatments of rheumatoid arthritis (RA) and other chronic inflammatory diseases.

Complete Freund's adjuvant suppresses the development and progression of pristane-induced arthritis in rats.

The present study produced the novel finding that treatment with a nonarthritogenic dose of Complete Freund's adjuvant (CFA) before the onset of pristane-induced arthritis (PIA) could prevent the development of PIA. Surprisingly, treatment with nonarthritogenic and arthritogenic doses of CFA could almost cure the ongoing PIA. CFA treatment also suppressed pathological changes, such as inflammatory cell infiltration, pannus formation, bone destruction, and new bone formation. The lymph node cells of rats with PIA suppressed by CFA showed significantly increased mRNA expression of IFN-gamma but no significant changes in mRNA expression of IL-2, TNF-alpha, IL-4, and IL-5 compared with those of rats in the control groups. The possible mechanisms of the suppressive effect of CFA on the development and progression of PIA were discussed in terms of the anti-inflammatory roles of IFN-gamma, nitric oxide, and heat-shock protein-specific T cell responses. The present study found a new therapeutic implication for the treatment of rheumatoid arthritis.