Anti-TLR4 Monoclonal antibody, clone NUT620

Background Toll-like receptor 4 (rs4986790, rs4986791) single nucleotide polymorphisms (SNPs) have been shown to be associated with age-related macular degeneration (AMD), but the results are still inconclusive. The present meta-analysis was conducted to evaluate the association between SNPs of TLR4 gene and AMD susceptibility. Methods Relevant articles were obtained through computer retrieval of Pubmed, Embase, Chinese National Knowledge Infrastructure and China wanfang database. Eligible articles were selected according to the inclusion and exclusion criteria, and quality scores were made for them by NOS-scale. Relevant data were extracted for meta-analysis. The combined OR value and 95% confidence interval were used to evaluate the strength of the correlation. Funnel plot and Egger's regression were used to evaluate publication bias. All analyses were performed using STATA 11.0 software. Results A total of nine case-control studies were included in this meta-analysis. After combination, an significant association was found between rs4986790 polymorphism and AMD susceptibility in heterozygote model (AG vs. AA, OR = 1.400, 95%CI = 1.049-1.867,P= .022) and dominant model (GG+AG vs. AA, OR = 1.365, 95%CI = 1.028-1.813,P= .032). There was no association found between rs4986791 polymorphism and AMD susceptibility in all genetic models (allP> .05). Funnel plot and Egger's regression analysis showed no publication bias existed in this study. Conclusions Meta-analysis suggested that there is an association between TLR4 gene rs4986790 polymorphism and AMD susceptibility, while no association between rs4986791 polymorphism and AMD susceptibility.

Euterpe oleraceaMart., commonly known as acai, has been demonstrated to exhibit significantly antioxidant and inflammatory activities in experimental models. These effects of the hydroalcoholic extract from the acai seed (ASE) were investigated in TNBS-induced (2,4,6-trinitrobenzenesulfonic acid) acute colitis model in rats. Wistar rats (180-220 g) were orally pretreated with saline (0.3 mL), ASE (10, 30 and 100 mg/kg) and dexamethasone (control group, 1 mg/kg) once daily for 3 days starting before TNBS instillation. On day 3 after TNBS, the animals were euthanized, the portion of distal colon was collected and washed with 0.9% saline for macroscopy and histological evaluation, glutathione (GSH) and malonyldialdehyde (MDA) levels, myeloperoxidase (MPO) and catalase (CAT) activity, nitrate and nitrite (NO3/NO2) concentration, pro-inflammatory cytokines levels and intestinal barrier integrity. We also evaluated Toll-like Receptor 4/cyclooxygenase-2/nuclear factor kappa B expression as a possible mechanism related to the ASE effects. Treatment with ASE 100 mg/kg decreased significantly macroscopic and microscopic damage induced by TNBS. In addition, MPO activity, TNF-alpha (tumor necrosis factor-alpha) and IL-1 beta (interleukin 1) levels were reduced in rats with colitis. ASE 100 mg/kg restored GSH and MDA levels, CAT activity, NO3/NO(2)concentration and improved the intestinal barrier integrity in the TNBS group. ASE 100 mg/kg significantly reduced TNBS-induced expression of the TLR4, COX-2 and NF-kappa B p65. ASE 100 mg/kg improved macroscopy and histological parameters, inflammation, intestinal barrier integrity and nitric and oxidative stress through the TLR-4/COX-2/NF-kappa B pathway.