Effects of Vam3 on sodium nitroprusside-induced apoptosis and SIRT1 and p53 expression in rat articular chondrocytes / 药学学报
Acta Pharmaceutica Sinica
;
(12): 608-614, 2014.
Article
in Chinese
| WPRIM
| ID: wpr-245039
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Nitroprusside
/
Cartilage, Articular
/
Cells, Cultured
/
Tumor Suppressor Protein p53
/
Reactive Oxygen Species
/
Rats, Wistar
/
Apoptosis
/
Chondrocytes
/
Nitric Oxide Donors
Limits:
Animals
Language:
Chinese
Journal:
Acta Pharmaceutica Sinica
Year:
2014
Type:
Article
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