Effects of 18β-Glycyrrhetinic acid in hTNFtg mice - a model of rheumatoid arthritis.
BACKGROUND
Rheumatoid arthritis is a chronic autoimmune disease characterised by inflammation of joints with cartilage and bone destruction leading to progressive disability. While the cause of rheumatoid arthritis is not known and the disease cannot be cured, conventional disease modifying antirheumatic drugs and biologicals are effective treatments for many patients. However, new therapies are needed in order to achieve better relief from rheumatoid arthritis symptoms than currently possible and to fully prevent joint damage. 18β-Glycyrrhetinic acid is not only used frequently in traditional Chinese medicine, but has been reported to target some of the inflammatory mediators involved in the pathogenesis of rheumatoid arthritis. Moreover, it has been reported that liquorice, which contains high levels of 18β-Glycyrrhetinic acid, reduces inflammation and articular damage in collagen induced arthritis. Therefore, we studied the effects of 18β-Glycyrrhetinic acid in a Tumor necrosis factor (TNF) dependent mouse model of rheumatoid arthritis.


METHODS
HTNFtg mice were treated with 18ß-Glycyrrhetinic acid from day 28 after birth every second or third day for 2 weeks, or 3 times a week for six weeks. TNF inhibitor treated animals served as positive control.


RESULTS
Clinical scores of arthritis were not altered in animals treated with 18β-Glycyrrhetinic acid compared to placebo treated animals. Histological data also indicate no effects of 18β-Glycyrrhetinic acid on inflammatory joint destruction. TNF inhibitors, however markedly reduced not only clinical signs of TNF triggered joint inflammation but also histological signs of erosive disease. Therefore, in contrast to previous reports our data indicate that 18β-Glycyrrhetinic acid does not provide a new therapeutic option for treating patients with rheumatoid arthritis.
Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna, Vienna, Austria.
Antonia
A
Puchner
Silvia
S
Hayer
Birgit
B
Niederreiter
Anastasiya
A
Hladik
Stephan
S
Blueml
Michael
M
Bonelli
Clemens
C
Scheinecker
Josef
J
Smolen
Kurt
K
Redlich
D000818:Animals; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000473:pathology*; D004195:Disease Models, Animal; D006034:Glycyrrhetinic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; C119129:18alpha-glycyrrhetinic acid; D006034:Glycyrrhetinic Acid