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Equol suppresses inflammatory response and bone erosion due to rheumatoid arthritis in mice.
- Source :
-
Journal of Nutritional Biochemistry . Jun2016, Vol. 32, p101-106. 6p. - Publication Year :
- 2016
-
Abstract
- Rheumatoid arthritis (RA) is a chronic and systemic autoimmune inflammatory disease. Typical pathological findings of RA include persistent synovitis and bone degradation in the peripheral joints. Equol, a metabolite of the major soybean isoflavone daidzein, shows superior bioactivity than other isoflavones. We investigated the effects of equol administration on inflammatory response and bone erosion in mice with collagen-induced arthritis (CIA). The severity of arthritis symptoms was significantly low in the equol-administered CIA mice. In addition, equol administration improved the CIA-induced bone mineral density decline. In the inflamed area of CIA mice, equol administration suppressed the expression of interleukin-6 and its receptor. Furthermore, equol reduced the expression of genes associated with bone formation inhibition, osteoclast and immature osteoblast specificity and cartilage destruction. These results suggest that equol suppresses RA development and RA-induced bone erosion by regulating inflammation and bone metabolism. [ABSTRACT FROM AUTHOR]
- Subjects :
- *DAIDZEIN
*INFLAMMATION prevention
*RHEUMATOID arthritis treatment
*AUTOIMMUNE diseases
*DRUG administration
*LABORATORY mice
*BONE metabolism
*NONSTEROIDAL anti-inflammatory agents
*PROTEIN metabolism
*THERAPEUTIC use of isoflavones
*PHYTOESTROGENS
*ANIMAL experimentation
*BIOCHEMISTRY
*BIOLOGICAL models
*BONE resorption
*BONES
*CELL receptors
*COMPUTED tomography
*DIETARY supplements
*GLYCOPROTEINS
*IMMUNITY
*INTERLEUKINS
*PHENOMENOLOGY
*MICE
*OSTEOCHONDROSIS
*PHOSPHOPROTEINS
*PROTEINS
*RHEUMATOID arthritis
*BONE density
*SYNOVITIS
*CHEMICAL inhibitors
*PREVENTION
*THERAPEUTICS
Subjects
Details
- Language :
- English
- ISSN :
- 09552863
- Volume :
- 32
- Database :
- Academic Search Index
- Journal :
- Journal of Nutritional Biochemistry
- Publication Type :
- Academic Journal
- Accession number :
- 115413584
- Full Text :
- https://doi.org/10.1016/j.jnutbio.2016.02.012