First Author | Tsuji G | Year | 2006 |
Journal | Free Radic Biol Med | Volume | 40 |
Issue | 10 | Pages | 1721-31 |
PubMed ID | 16678011 | Mgi Jnum | J:108825 |
Mgi Id | MGI:3624930 | Doi | 10.1016/j.freeradbiomed.2006.01.006 |
Citation | Tsuji G, et al. (2006) Thioredoxin protects against joint destruction in a murine arthritis model. Free Radic Biol Med 40(10):1721-31 |
abstractText | Thioredoxin (TRX) is an oxidative stress-inducible biological antioxidant that is highly expressed in the synoviocytes of rheumatoid arthritis (RA) patients. There is much evidence that oxidative stress plays a key role in the inflammation and destruction of RA joints; the functional relationship between TRX and RA remains unknown, however. We therefore investigated the role played by TRX in the inflammatory and joint-damaging processes of RA using a murine model in which arthritis was induced by administering a mixture of anti-type II collagen monoclonal antibodies (mAb) and lipopolysaccharide (LPS). In Wt mice mAb/LPS injection induced neutrophil infiltration, cartilage destruction, and chondrocyte apoptosis within the joints, all of which were dramatically suppressed in TRX transgenic (TRX-Tg) mice. Moreover, the 8-hydoxy-2'-deoxyguanosine (8-OHdG) expression seen in Wt mice after mAb/LPS injection was almost completely inhibited in TRX-Tg mice. The administration of recombinant TRX also suppressed mAb/LPS-induced joint swelling in Wt mice. Taken together, these results suggest that TRX protects against arthritis and is a plausible candidate with which to develop novel therapies for the treatment of RA. |