Yamagishi Yoshie, Someya Akimasa, Nagaoka Isao
Department of Host Defense and Biochemical Research, Juntendo University, Graduate School of Medicine, Tokyo 113-8421, Japan.
Biomed Rep. 2020 Jul;13(1):37-42. doi: 10.3892/br.2020.1304. Epub 2020 May 12.
The aim of the present study was to evaluate the anti-inflammatory effects of citrulline (Cit), glucosamine (GlcN) and N-acetylglucosamine (GlcNAc) on synovial cells, which are primarily involved in inflammatory joint diseases. The combined effect of Cit, GlcN and GlcNAc on synovial cell inflammation was assessed by measuring IL-1β-induced IL-6 production. GlcN and GlcNAc (0.5 mM each) alone did not suppress IL-6 production, whereas Cit (0.5 mM) did significantly suppress IL-6 production. Furthermore, the combined effect of Cit, GlcNAc and GlcN was examined; Cit + GlcN and Cit + GlcNAc significantly suppressed not only IL-6 production, but also phosphorylation of ERK1/2. Similarly, combination of GlcN + GlcNAc significantly suppressed IL-6 production and phosphorylation of ERK1/2. These observations suggest that among Cit, GlcNAc and GlcN, the combination of Cit with GlcN or GlcNAc exerts a synergistic anti-inflammatory effect on synovial cells, thereby possibly exhibiting chondroprotective effects and alleviating inflammatory joint diseases.
本研究的目的是评估瓜氨酸（Cit）、氨基葡萄糖（GlcN）和N - 乙酰氨基葡萄糖（GlcNAc）对滑膜细胞的抗炎作用，滑膜细胞主要参与炎症性关节疾病。通过测量白细胞介素 - 1β（IL - 1β）诱导的白细胞介素 - 6（IL - 6）产生来评估Cit、GlcN和GlcNAc对滑膜细胞炎症的联合作用。单独的GlcN和GlcNAc（各0.5 mM）不抑制IL - 6的产生，而Cit（0.5 mM）确实显著抑制IL - 6的产生。此外，还研究了Cit、GlcNAc和GlcN的联合作用；Cit + GlcN和Cit + GlcNAc不仅显著抑制IL - 6的产生，还抑制细胞外信号调节激酶1/2（ERK1/2）的磷酸化。同样，GlcN + GlcNAc的组合也显著抑制IL - 6的产生和ERK1/2的磷酸化。这些观察结果表明，在Cit、GlcNAc和GlcN中，Cit与GlcN或GlcNAc的组合对滑膜细胞具有协同抗炎作用，从而可能具有软骨保护作用并减轻炎症性关节疾病。
