Resveratrol Inhibits Nitric Oxide-Induced Apoptosis via the NF-Kappa B Pathway in Rabbit Articular Chondrocytes.
- Author:
Seong Hui EO
1
;
Hongsik CHO
;
Song Ja KIM
Author Information
1. Department of Biological Sciences, College of Natural Sciences, Kongju National University, Gongju 314-701, Republic of Korea. ksj85@kongju.ac.kr
- Publication Type:Original Article
- Keywords:
Resveratrol;
Chondrocytes;
Nitric oxide;
Sodium nitroprusside;
Apoptosis;
NF-kappa B
- MeSH:
Apoptosis*;
Blotting, Western;
Caspase 3;
Chondrocytes*;
Humans;
I-kappa B Proteins;
Inflammation;
Microscopy, Phase-Contrast;
NF-kappa B*;
Nitric Oxide;
Nitroprusside;
Tissue Donors;
Vitis;
Wine
- From:Biomolecules & Therapeutics
2013;21(5):364-370
- CountryRepublic of Korea
- Language:English
-
Abstract:
Resveratrol (trans-3,4'-trihydroxystillbene), a naturally occurring polyphenolic antioxidant found in grapes and red wine, elicits diverse biochemical responses and demonstrates anti-aging, anti-inflammatory, and anti-proliferative effects in several cell types. Previously, resveratrol was shown to regulate differentiation and inflammation in rabbit articular chondrocytes, while the direct production of nitric oxide (NO) in these cells by treatment with the NO donor sodium nitroprusside (SNP) led to apoptosis. In this study, the effect of resveratrol on NO-induced apoptosis in rabbit articular chondrocytes was investigated. Resveratrol dramatically reduced NO-induced apoptosis in chondrocytes, as determined by phase-contrast microscopy, the MTT assay, FACS analysis, and DAPI staining. Treatment with resveratrol inhibited the SNP-induced expression of p53 and p21 and reduced the expression of procaspase-3 in chondrocytes, as detected by western blot analysis. SNP-induced degradation of I-kappa B alpha (IkappaB-alpha) was rescued by resveratrol treatment, and the SN50 peptide-mediated inhibition of NF-kappa B (NF-kappaB) activity potently blocked SNP-induced caspase-3 activation and apoptosis. Our results suggest that resveratrol inhibits NO-induced apoptosis through the NF-kappaB pathway in articular chondrocytes.
