The chronic effect of palmitic acid on apoptosis of pancreatic islet beta-cells and the mechanism.
- Author:
Liang LIU
1
;
Ran-Ping WANG
;
Xiao-Hong LIU
;
Lin-Xi WANG
;
Xiao-Ying LIU
;
Wen-Jia CHEN
;
Li-Bin LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Cell Line, Tumor; Cells, Cultured; Insulinoma; pathology; Islets of Langerhans; pathology; Mice; Oxidative Stress; physiology; Palmitic Acid; pharmacology; Proto-Oncogene Proteins; metabolism; Proto-Oncogene Proteins c-akt; metabolism; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; drug effects; physiology; bcl-2-Associated X Protein; metabolism
- From: Chinese Journal of Applied Physiology 2009;25(4):553-556
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the chronic effect of palmitic acid (PA) on apoptosis of pancreatic islet beta-cells and the possible mechanism.
METHODSInsulinoma cell line (MIN6 cells) were used in this study. After being incubated in PA (0.1 - 1.6 mml/L) for 24 and 48 hours, MTT method was used to evaluate the livability. After being incubated for 48 h, Hoechst-PI and Annexin-V-FTTC/PI FACS were used to estimate the apoptosis in each group, Western-blotting assay was used to estimate the protein level of p-Akt, Akt, Bax and Bcl-2.
RESULTSChronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax.
CONCLUSIONChronic PA dose-dependently induced apoptosis of MIN6 cells, and this effect was possibly regulated by Akt/Bcl-2.
