Effects of hydrogen-rich medium on cellular oxidative products and antioxidant status. Sample histographs comparing the H2O2 treatment, H2 treatment increased SOD level and decreased GSH level. 8-OHdG levels decreased in H2 treatment group following treatment time. (V represents H2O2 group, H represents H2O2 and hydrogen group, 1 represents 24 h, 2 represents 48 h, 3 represents 72 h and N represents normal control).
Outcomes of cures which have hydrogen into MAPKs and you will NF-?B pathway
NF-?B transcription family plays an important role in the inflammatory response of RA progression. MAPKs extensively regulate RA-related events, especially in the expressions of proteases. As predicted, exposure of H2 decreased significantly the MAPKs and NF-?B activation in RA-FLSs ( Figure 5 ). These results indicate that H2 might inhibit the inflammation process in H2O2-treated RA-FLSs by regulating the intracellular MAPK and NF-?B pathways.
Effects of hydrogen treatment on MAPKs and NF-?B pathway. Representative histographs showing that exposure to H2 decreased MAPKs and NF-?B activation in RA-FLSs significantly, compared with other groups. (V represents H2O2 group, H represents H2O2 and hydrogen group, 1 represents 24 h, 2 represents 48 h, 3 represents 72 h and N represents normal control).
Effects of treatment which have hydrogen on TGF-?1 phrase
TGF-?1 regulates cell growth, adhesion and differentiation in a variety of cell types. We assessed the effect of H2 on TGF-?1 activation in synovial cells. Pre-incubation of RA-FLSs with H2O2 elevated TGF-?1 expression within the cytosol and decreased TGF-?1 expression with H2. The H2O2 effect was significantly reversed by H2 ( Figure 6 ).
Pre-incubation of RA-FLSs with H2O2 elevated TGF-?1 expression within the cytosol and decreased TGF-?1 expression with H2. Histogram showing the effect of H2O2 was significantly reversed by H2. (V represents H2O2 group, H represents H2O2 and hydrogen group, 1 represents 24 h, 2 represents 48 h, 3 represents 72 h and N represents control).
Talk
In this paper, we showed that H2 exerted therapeutic effects in a mouse model of RA and in human RA-FLS cells. The probable mechanisms of action of H2 were also further elucidated. Our data suggested that H2 could reduce the levels of oxidative products and attenuate H2O2 – induced over proliferation in RA-FLSs.