Effect of Par-4 on the apoptosis of islet β cell.
10.11817/j.issn.1672-7347.2015.01.002
- Author:
Xiaguang GAN
1
;
Qi'nan WU
;
Wuquan DENG
;
Ling ZHANG
;
Bing CHEN
Author Information
1. Department of Endocrinology, First Affi liated Hospital, Third Military Medical University, Chongqing 400038, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Apoptosis Regulatory Proteins;
metabolism;
Cell Line;
Fatty Acids;
Gene Expression Regulation;
Glucose;
Heat-Shock Proteins;
metabolism;
In Situ Nick-End Labeling;
Islets of Langerhans;
cytology;
Mice
- From:
Journal of Central South University(Medical Sciences)
2015;40(1):6-11
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the effect of high glucose and lipid intervention on islet cell apoptosis through the inhibition of prostate apoptosis response factor-4 (Par-4) expression and the underlying mechanisms.
METHODS:The mice islet β cells (NIT-1 cells) were randomly divided into a control group, a Par-4 inhibited group, a glucose and fatty acid intervented group and a glucose and fatty acid intervented+Par-4 inhibited group. Cell apoptosis was detected by terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL), and the protein expression levels of Par-4 and glucose regulated protein 78 (GRP78) were detected by Western blot.
RESULTS:Compared with the control group [(3.14 ± 1.08)%], the apoptosis rate of islet beta cell [(33.82 ± 3.15)%] in the glucose and fatty acid intervented group was significantly increased accompanied by the dramatically elevated Par-4 and GRP78 expression (both P<0.05). Compared with the glucose and fatty acid intervented group, the apoptosis rate in glucose and fatty acid intervented+Par-4 inhibit group [(18.3 4 ± 2.11)%] was significantly decreased concomitant with the significantly decreased Par-4 and GRP78 expression (both P<0.05).
CONCLUSION:The glucose and fatty acid-induced apoptosis of mice islet β cells could be improved through the inhibition of Par-4 expression, which might be related to reduction of endoplasmic reticulum stress.
