Effect of high glucose peritoneal dialysis solution on PGC-1α expression and mitochondria related oxidative injury in human peritoneal mesothelial cells.
10.3969/j.issn.1672-7347.2013.11.001
- Author:
Xuejing ZHU
1
;
Feng WEN
;
Danyi YANG
;
Jing LIU
;
Shuguang YUAN
;
Jun LI
;
Hong LIU
;
Xiangqing XU
;
Lin SUN
;
Fuyou LIU
Author Information
1. Department of Nephrology, Second Xiangya Hospital, Central South University; Kidney Institute, Central South University; Key Lab of Kidney Disease and Dialysis of Hunan Province, Changsha 410011, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Dialysis Solutions;
adverse effects;
Epithelial Cells;
pathology;
Glucose;
adverse effects;
Humans;
Mitochondria;
metabolism;
pathology;
Oxidative Stress;
Peritoneal Dialysis;
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha;
Reactive Oxygen Species;
Transcription Factors;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2013;38(11):1085-1091
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the mechanism of mitochondrial oxidative injury induced by high glucose peritoneal dialysis solution (PDS) and the protective effect of peroxisome proliferator activated receptor gamma coactivator 1-alpha (PGC-1α) in the mitochondria of human peritoneal mesothelial cells (HPMC) in the high glucose ambience.
METHODS:HPMC was cultured in a PDS containing 1.5%, 2.5% and 4.25% glucose for 24 hours. Western blot analysis was used to detect PGC-1α expression. MitoSOX? Red staining, respiratory chain complexes and antioxidant enzyme activities were determined.
RESULTS:The activities of respiratory chain complex III and antioxidant enzymes decreased significantly in a concentration- and time-dependent manner, along with the increased production of mitochondrial reactive oxygen species (ROS) and cellular apoptosis. In addition, protein expression of PGC-1α was also decreased in the high glucose PDS ambience.
CONCLUSION:High glucose PDS might inhibit PGC-1α expression, resulting in the inhibition of mitochondrial function and increase of mitochondrial ROS and cellular apoptosis.
