By a News Reporter-Staff News Editor at Biotech Week -- A new study on Arthritis is now available. According to news originating from Baltimore, Maryland, by NewsRx correspondents, research stated, "Inflammation and tissue degeneration play key roles in numerous rheumatic diseases, including osteoarthritis (OA). Efforts to reduce and effectively repair articular cartilage damage in an osteoarthritic environment are limited in their success due to the diseased environment."
Our news journalists obtained a quote from the research from Johns Hopkins University, "Treatment strategies focused on both reducing inflammation and increasing tissue production are necessary to effectively treat OA from a tissue-engineering perspective. In this work, we investigated the anti-inflammatory and tissue production capacity of a small molecule 3,4,6-O-tributanoylated-N-acetylglucosamine (3,4,6-O-Bu(3)GlcNAc) previously shown to inhibit the nuclear factor kappa B (NF kappa B) activity, a key transcription factor regulating inflammation. To mimic an inflammatory environment, chondrocytes were stimulated with interleukin-1 beta (IL-1 beta), a potent inflammatory cytokine. 3,4,6-O-Bu(3)GlcNAc exposure decreased the expression of NF kappa B target genes relevant to OA by IL-1 beta-stimulated chondrocytes after 24 h of exposure. The capacity of 3,4,6-O-Bu(3)GlcNAc to stimulate extracellular matrix (ECM) accumulation by IL-1 beta-stimulated chondrocytes was evaluated in vitro utilizing a three-dimensional hydrogel culturing system. After 21 days, 3,4,6-O-Bu(3)GlcNAc exposure induced quantifiable increases in both sulfated glycosaminoglycan and total collagen. Histological staining for proteoglycans and type II collagen confirmed these findings. The increased ECM accumulation was not due to the hydrolysis products of the small molecule, n-butyrate and N-acetylglucosamine (GlcNAc), as the isomeric 1,3,4-O-tributanoylated N-acetylglucosamine (1,3,4-O-Bu(3)GlcNAc) did not elicit a similar response."
According to the news editors, the research concluded: "These findings demonstrate that a novel butanoylated GlcNAc derivative, 3,4,6-O-Bu(3)GlcNAc, has the potential to stimulate new tissue production and reduce inflammation in IL-1 beta-induced chondrocytes with utility for OA and other forms of inflammatory arthritis."
For more information on this research see: Short-Chain Fatty Acid-Modified Hexosamine for Tissue-Engineering Osteoarthritic Cartilage. Tissue Engineering Part A, 2013;19(17-18):2035-2044. Tissue Engineering Part A can be contacted at: Mary Ann Liebert, Inc, 140 Huguenot Street, 3RD Fl, New Rochelle, NY 10801, USA (see also Arthritis).
The news correspondents report that additional information may be obtained from J.M. Coburn, Johns Hopkins University, Dept. of Med, Div Rheumatol, Baltimore, MD 21287, United States. Additional authors for this research include L. Wo, N. Bernstein, R. Bhattacharya, U. Aich, C.O. Bingham, K.J. Yarema and J.H. Elisseeff.
Keywords for this news article include: Tissue Engineering, Biomedical Engineering, Biomedicine, Maryland, Genetics, Baltimore, Inflammation, United States, Bioengineering, Osteoarthritis, North and Central America
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