Biliverdin protects against cisplatin-induced apoptosis of renal tubular epithelial cells.
10.1007/s11596-016-1540-8
- Author:
Qian LV
1
;
Ying YAO
2
;
Wei WANG
3
;
Wei XIONG
4
;
Wen-hui LIAO
5
Author Information
1. Department of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. e21195552@126.com.
2. Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
3. Department of Hepatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
4. Department of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
5. Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. Liaowh126@126.com.
- Publication Type:Journal Article
- Keywords:
apoptosis;
biliverdin;
cisplatin;
reactive oxygen species
- MeSH:
Animals;
Antioxidants;
pharmacology;
Apoptosis;
Biliverdine;
pharmacology;
Cell Line;
Cisplatin;
toxicity;
Epithelial Cells;
drug effects;
metabolism;
Kidney Tubules;
cytology;
Rats;
Reactive Oxygen Species;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(1):48-52
- CountryChina
- Language:English
-
Abstract:
Biliverdin (BV) has long been thought to be a cytotoxic metabolic waste product. It has also been demonstrated to have important cytoprotective functions during oxidative stress. The present study aimed to examine the cytoprotective effect of BV on NRK-52E cells, a proximal tubular cell line derived from rat kidney. Cells were treated with 50 µmol/L cisplatin for 24 h (cisplatin group) or pre-treated with BV for 30 min, then with 50 µmol/L cisplatin for 24 h (cisplatin+BV group). Those given no treatment served as a control. Cell apoptosis was evaluated by flow cytometry and cell viability by Cell Counting Kit-8 (CCK-8). The protein expressions of cleaved caspase3, Bax and Bcl-2 were assessed by Western blotting. Reactive oxygen species (ROS) levels were measured using carboxydichlorodihydrofluorescein diacetate (H2DCF). The results showed that cisplatin induced the apoptosis of NRK-52E cells, decreased cell viability, and increased the formation of ROS by upregulating the expression of cleaved caspase3 and Bax and decreasing Bcl-2 protein expression. These effects could be significantly reversed by pretreatment with BV. It was concluded that BV can protect against cisplatin-induced cell apoptosis through the anti-oxidative effects.
