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
,
2
,
3
;
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
2. Kidney Institute, Central South University
3. 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.
