摘要
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.
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.
