Effect and underlying mechanism of resveratol on porcine primary preadipocyte apoptosis.
- Author:
Zhao ZHANG
1
;
Yang YANG
;
Weijun PANG
;
Chao SUN
;
Gongshe YANG
Author Information
1. Laboratory of Animal Fat Deposition and Muscle Development, Northwest A&F University, Yangling 712100, China.
- Publication Type:Journal Article
- MeSH:
Adipocytes;
cytology;
Adipogenesis;
Animals;
Antioxidants;
pharmacology;
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Cells, Cultured;
Sirtuin 1;
metabolism;
Stilbenes;
pharmacology;
Swine
- From:
Chinese Journal of Biotechnology
2010;26(8):1042-1049
- CountryChina
- Language:Chinese
-
Abstract:
We demonstrated the effect of resveratrol on porcine primary preadipocytes apoptosis, to study the intracellular molecular mechanism. Porcine primary preadipocyte was treated with different concentration of resveratrol (0 micromol/L, 50 micromol/L, 100 micromol/L, 200 micromol/L, 400 micromol/L). We used optical microscope and fluorescence microscope to observe morphological changes during apoptosis after Hoechst 33258 Fluorescent dyes staining; and RT-PCR and Western blotting to measure the expression of apoptosis-associated gene sirt1, caspase-3, bcl-2, bax, p53, NF-kappaB. Primary preadipocyte apoptosis was apparent, accompanied by reduced cell volume, chromatin condensation, and nuclear shrinkage. Compared to the control and low concentration group, high dose group (200 micromol/L) significantly increased the ratio of primary preadipocyte apoptosis. The expression of sirt1, caspase-3, and bax was up-regulated markedly in response to resveratrol; in contrast, apoptotic inhibitor bcl-2, p53, NF-kappaB down-regulated. We further proved fact that resveratrol can specifically promote the activity of sirt1; moreover, activated sirt1 modulates the activity of caspase-3 and bcl-2 family, involving in transcriptional regulation of p53 and NF-kappaB through antagonizing factor-induced acetylation. Taken together, our data established resveratrol as new regulator in porcine primary preadipocyte apoptosis via activating the expression of sirt1, modulating activity of apoptotic-associated factor.
