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Melatonin‐mediated suppression of early peripheral sensitization in osteoarthritic meniscus
Author(s) -
Hong Yunkyung,
Kim JooHeon,
Hong Yonggeun
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb438
Subject(s) - melatonin , nociception , sensitization , medicine , endocrinology , analgesic , pharmacology , peripheral , chemistry , receptor , immunology
Joint pain is classified as a major symptom in most of osteoarthritic (OA) cases. Most common management for OA is to alleviate symptoms through administration with conventional analgesic drugs, but patients continued to experience pain. Therefore, the present study is aimed at determining the effects of melatonin on peripheral nociceptive processing in animals with collagenase‐induced cartilage damage. Melatonin (10 mg/kg) was injected twice daily subcutaneously. There was TrkB upregulation as well as increase of non‐glycosylated NK‐1R despite no difference of its glycosylation in OA meniscus, but melatonin blocked it. To study the effect of melatonin on cells exposed to inflammatory neuropeptides, primary cultured chondrocytes were treated with both TNF‐α and rCGRP. Increase of Bax/Bcl‐2 ratio is accompanied by reduction of cell viability, and there were a loss of type II collagen, increase of active MMP‐13, and nuclear Ca 2+ deposition. But melatonin at the nanomolar concentration rescued from damage responses. These molecular results might indicate early anti‐nociceptive effect of melatonin, but behavior of the animals was deemed hypersensitive to innocuous mechanical stimuli. Further experiments are needed to elucidate their inconsistency. Funding: 2012R1A1A2005089, 2013R1A2A2A01067169, KGM4611512