Effects of Vam3 on sodium nitroprusside-induced apoptosis and SIRT1 and p53 expression in rat articular chondrocytes.
- Author:
Ren-Tao JIANG
;
Chun-Suo YAO
;
Jin-Ye BAI
;
Qi HOU
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Arabidopsis Proteins;
pharmacology;
Cartilage, Articular;
cytology;
Caspase 3;
metabolism;
Caspase 9;
metabolism;
Cells, Cultured;
Chondrocytes;
cytology;
metabolism;
Male;
Membrane Potential, Mitochondrial;
drug effects;
Nitric Oxide Donors;
antagonists & inhibitors;
pharmacology;
Nitroprusside;
pharmacology;
Qa-SNARE Proteins;
pharmacology;
Rats;
Rats, Wistar;
Reactive Oxygen Species;
metabolism;
Sirtuin 1;
metabolism;
Tumor Suppressor Protein p53;
metabolism
- From:
Acta Pharmaceutica Sinica
2014;49(5):608-614
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate the effect of Vam3, a dimeric derivative of resveratrol, on SNP-induced apoptosis and its potential mechanism in rat articular chondrocytes. Isolated rat articular chondrocytes were treated with sodium nitroprusside (SNP), a NO donor, to induce apoptosis. Apoptosis percentage was evaluated by Annexin V-PI and nucleus fracture was examined by DAPI staining. Level of intracellular reactive oxygen species (ROS) was detected using 2, 7'-dichlorofluorescin diacetate (DCFH-DA) as a fluorescence probe by fluorescence microplate reader. The change in mitochondrial membrane potential was detected by TMRE staining. Expressions of SIRT1, acetylated p53 (ac-p53), cleaved caspase 9 and cleaved caspase 3 were determined by Western blotting. It showed that Vam3 up to 10 micromol x L(-1) could significantly reduce SNP-induced rat articular chondrocytes apoptosis (P < 0.01) and nucleus fracture, inhibit the increase of intracellular ROS level (P < 0.01) and reverse the decrease in mitochondrial membrane potential (P < 0.01). Simultaneously, Vam3 could upregulate the expression of SIRT1, deacetylate p53, and inhibit the cleavage of caspase 9 and caspase 3 (P < 0.01) of rat articular chondrocytes exposed to SNP. This study indicates Vam3 could protect rat articular chondrocytes against SNP-induced apoptosis, perhaps through the upregulation of SIRT1 and deacetylation of p53.
