Figure 4
Renogrit decreased cisplatin-induced oxidative stress and mitochondrial dysfunction in HK-2 cells. (a) The reactive oxygen species (ROS) burst generated in response to HK-2 cells induced with cisplatin at human Cmax (15 µg/ml) was inhibited in presence of Renogrit (10–100 µg/ml). Prior to fluorescence measurements, H2DCFDA stained HK-2 cells were simultaneously treated with cisplatin and Renogrit or NAC (2 mM) and the converted DCF was evaluated for 120 min. (b) Renogrit treatment normalized the GST levels in HK-2 cells that were altered in response to cisplatin induction. (c) Renogrit treatment enhanced the mitochondrial membrane potential of HK-2 cells which was decreased in response to cisplatin induction as observed by ratiometric fluorescence measurements of cells stained with JC-1. Data represented as mean ± S.E.M. ### and ***p < 0.001; ## and **p < 0.01.
