Search

Objective The main purpose of the present study was to define the impact of high-dose of 365 ± 5 nm ultraviolet A1 (UVA1) on dermal fibrosis in the pre-established, bleomycin-induced mouse model of scleroderma. Methods DBA/2 strain mice with the pre-established, bleomycin-induced scleroderma were irradiated with cumulative UVA1 dose of 1200 J/cm 2 and in parallel were challenged with prolonged administration of bleomycin. Non-treated groups served as the control. Light source emitting a narrow band UVA1 light of 365 ± 5 nm and 21 mW/cm 2 power density was used in the study. Histological analysis was performed for the evaluation of dermal thickness. The expressions of matrix-metalloproteinase-1 (MMP-1), matrix-metalloproteinase-3 (MMP-3), collagen types I and III were evaluated by immunohistochemical analyses. The Mann - Whitney U test was used for statistical analysis. Results Dermal thickness in mice injected with bleomycin during all the experiment (8 weeks) and irradiated with UVA1 for the last 5 weeks was significantly lower than that in mice challenged only with bleomycin for 8 weeks (253.96 ± 31.83 μm and 497.43 ± 57.83 μm, respectively; P = 0.002). The dermal thickness after phototherapy was lower as compared with the pre-existing fibrotic changes observed after 3 weeks of bleomycin injections (253.96 ± 31.83 μm and 443.87 ± 41.76 μm, respectively; P = 0.002). High-dose of UVA1 induced the 5.8- and 5.2-fold increase in MMP-1 and MMP-3 expressions, respectively, and the 1.2- and 1.4-fold decrease in collagen type I and collagen type III expressions in the pre-established, bleomycin-induced scleroderma model as compared to that in the control non-irradiated mice ( P = 0.002). Conclusions Our study has demonstrated that a cumulative 365 ± 5 nm UVA1 radiation dosage of 1200 J/cm 2 not only prevents the progression of dermal fibrosis, but also induces a regression of pre-existing fibrotic changes. [ABSTRACT FROM AUTHOR]

Objective To compare the accumulation of protoporphyrin IX between synoviocytes of patients with rheumatoid arthritis (RA) or osteoarthritis (OA) and cartilage explants (CE) as well as chondrons of patients with OA after the application of 5-aminolevulinic acid (ALA) or its methyl ester (ALA-Me). Materials and methods Samples of synovial and cartilage tissues were obtained from joint replacement surgeries. The accumulation of PpIX was determined by measuring fluorescence spectra from 2 × 10 5 synoviocytes or chondrons suspended in a glass tube or directly from CE surface after 2, 4, 8 and 24 h of incubation with ALA or ALA-Me. Results No differences were found between the average fluorescence intensity values of PpIX in synoviocytes of patients with RA and OA. These values were non-significantly higher after incubation with ALA in comparison with ALA-Me at almost all time points. The average fluorescence intensity of PpIX in CE and chondrons was about ten times lower than in synoviocytes. The presence of preparation of hyaluronic acid (HA) significantly enhanced PpIX induction in chondrons versus treatment only with ALA. Conclusions A potential for the selective synovial sensitization with endogenous PpIX in comparison with cartilage tissue has been demonstrated in vitro after application of ALA or ALA-Me. [ABSTRACT FROM AUTHOR]