Biliverdin Protects against Cisplatin-induced Apoptosis of Renal Tubular Epithelial Cells

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-52 E cells, a proximal tubular cell line derived...

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Published inJournal of Huazhong University of Science and Technology. Medical sciences Vol. 36; no. 1; pp. 48 - 52
Main Author 吕倩 姚颖 王伟 熊薇 廖文慧
Format Journal Article
LanguageEnglish
Published Wuhan Huazhong University of Science and Technology 01.02.2016
Department of Hospital Infection Control,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China%Department of Nephrology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China%Department of Hepatic Surgery,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China%Department of Geriatrics,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China
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Summary: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-52 E 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-52 E 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.
Bibliography:42-1679/R
biliverdin cisplatin apoptosis reactive oxygen species
Qian LV , Ying YAO , Wei WANG , Wei XIONG , Wen-hui LIAO( 1Department of Hospital Infection Control 2Department of Nephrology, 3Department of Hepatic Surgery, 4Department of Geriatrics, Tongji Hospital Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China)
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-52 E 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-52 E 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.
ObjectType-Article-1
SourceType-Scholarly Journals-1
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content type line 23
ISSN:1672-0733
1993-1352
1993-1352
DOI:10.1007/s11596-016-1540-8