Suppression of inflammatory mediators and matrix metalloproteinase (MMP)-13 by Morus alba stem extract and oxyresveratrol in RAW 264.7â¯cells and C28/I2 human chondrocytes.
J Tradit Complement Med
; 10(2): 132-140, 2020 Mar.
Article
em En
| MEDLINE
| ID: mdl-32257876
ABSTRACT
This study aimed to investigate the effects of Morus alba stem extract (MSE) and oxyresveratrol on the suppression of pro-inflammatory mediators in LPS-stimulated RAW 264.7 macrophages and IL-1ß-stimulated C28/I2 human chondrocyte cell line. The chondroprotective effect was also investigated using the chondrocyte cell line. First, MSE was prepared and analyzed for the amount of oxyresveratrol. The anti-inflammatory effects of MSE at various concentrations were evaluated through the inhibition of nitric oxide (NO), prostaglandin (PG)-E2 and cyclooxygenase (COX)-2 production. Oxyresveratrol at the equivalent amount found in the extract was investigated in the same manner. The chondroprotective effect was investigated through the suppression of MMP-13 production. The results showed that oxyresveratrol content in MSE was 15%. In RAW 264.7â¯cells, MSE (5-50⯵g/mL) could inhibit the NO (24-30%) and PGE2 (11-82%) production. Oxyresveratrol at 0.75 and 7.5⯵g/mL could suppress NO and also inhibited PGE2 but at only at high concentration. In the chondrocyte cell line, MSE at 5-100⯵g/mL significantly decreased the PGE2 and COX-2 production by 44-93% and 17-65%, respectively. Again, oxyresveratrol at both concentrations could significantly inhibit PGE2 production by 50-92% but it inhibited COX-2 only at high concentration. In addition, MSE and oxyresveratrol was shown to significantly inhibit MMP-13 production by 14-57% and 16-56%, depending on their concentrations. The MSE demonstrates the potential to be used as an alternative treatment for reducing inflammation and preventing cartilage degradation. Its component, oxyresveratrol, may exert these effects to some extent.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article