![]() ![]() Randomization of rats to treatment groups was completed in which every other rat that developed signs of disease on a given day was placed in the same treatment group (PEG-HCC or vehicle), thereby removing differences in basal disease severity on the day each rat developed signs of disease and accounting for differences in the time between pristane injection and when a rat developed signs of disease. Rats were monitored daily, and clinical scores recorded as follows: 1 point for each swollen and red toe, midfoot, digit, or knuckle and 5 points for each swollen ankle or wrist for a maximum of 60 per rat. PIA was induced by the subcutaneous injection of 150 µL pristane (2,6,10,14-tetramethylpentadecane MP Biomedicals, Irvine, CA, USA) at the base of the tail. PIA was chosen as a model for this study because it mimics RA in humans in terms of involvement of FLS and immune cells, and production of rheumatoid factor. − and hydroxyl radicals in the pathogenesis of a rat model of RA and showed efficacy of PEG-HCCs in treating a rat model of RA.PEG-HCCs did not induce lymphopenia during PIA. In PIA, PEG-HCCs caused a 65% reduction in disease severity, as measured by a standardized scoring system of paw inflammation and caused a significant reduction in bone and tissue damage, and circulating rheumatoid factor. −, and reduced multiple measures of their pathogenicity in vitro, including proliferation and invasion.PEG-HCCs were internalized by RA-FLS, reduced their intracellular O 2 We used the pristane-induced arthritis (PIA) rat model of RA to assess the benefits of PEG-HCCs on reducing disease severity. We used human FLS from patients with RA to determine PEG-HCC internalization and effects on FLS cytotoxicity, invasiveness, proliferation, and production of proteases. −) and hydroxyl radicals with antioxidant nanoparticles, called poly(ethylene glycol)-functionalized hydrophilic carbon clusters (PEG-HCCs), on the pathogenic functions of fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA) and on the progression of an animal model of RA. ![]() Our goal was to determine the effects of selectively scavenging superoxide (O 2 Reactive oxygen species have been involved in the pathogenesis of rheumatoid arthritis (RA). ![]()
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