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Avenanthrimide C as a novel candidate of treatment to alleviate osteoarthritic pathogenesis
Thanh-Tam Tran1 (Graduate student), Won-Hyun Song1 (Researcher), Gyuseok Lee1 (Research Professor), Hyung Seok Kim2 (Professor), Daeho Park3 (Professor), Yun Hyun Huh3 (Professor), Je-Hwang Ryu 1,1,* (Professor)
1School of Dentistry, Chonnam National University,
2Department of Forensic Science, Chonnam National University Medical School,
3School of Life Sciences, Gwangju Institute of Science and Technology
Abstract
Osteoarthritis (OA) is the degenerative disorder which results in the loss of articular cartilage. No effective treatment against OA is currently available, thus the interest in natural health products to relieve symptoms is increasing. However, their quality, such as efficacy, toxicity, and mechanism, is poorly understood. In this study, we determined the efficacy of Avenanthrimide (Avn)-C extracted from oats as a promising candidate to prevent OA progression and its mechanism of action to prevent the expression of matrix-metalloproteinases (MMPs) in OA pathogenesis. Proinflammatory cytokine interleukin-1 beta (IL-1モ) as a main causing factor of cartilage destruction was used for the induction of in vitro OA-like condition of chondrocytes. Avn-C restrained IL-1モ-mediated expression and activity of MMPs, such as MMP-3, -12, and -13 in mouse articular chondrocytes. Moreover, Avn-C alleviated cartilage destruction in experimental OA mouse model induced by destabilization of the medial meniscus (DMM) surgery. However, Avn-C did not affect the expression of inflammatory mediators (Ptgs2 and Nos) and anabolic factors (Col2a1, Aggrecan, and Sox9), even though the expression of these genes was upregulated and downregulated by IL-1モ, respectively. The inhibition of MMP expression by Avn-C in articular chondrocytes was mediated by the p38 kinase and c-Jun N-terminal kinase (JNK) signaling but not ERK and NF-リB. Interestingly, Avn-C addition with the specific inhibitors of p38 kinase and JNK, SB203580 and SP600125, respectively, enhanced the inhibitory effect on the expression of MMPs in IL-1モ treated chondrocytes. Here, we suggest that Avn-C is a candidate as an effective treatment to prevent OA progression as well as a natural health product to relieve OA pathogenesis.
Abstract, Accepted Manuscript(in press) [Submitted on August 5, 2021, Accepted on August 26, 2021]
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