OBJECTIVE  To explore whether pyridoxine can protect acute kidney injury caused by cisplatin and to analyze its specific mechanism.

METHODS  After establishing an in vitro model of cisplatin-induced damage in HK-2 cells, different concentrations of pyridoxine were administered and cell survival was detected using SRB, the expression of apoptosis-related and antioxidant proteins were detected by Western blotting, and the activity of reactive oxygen species(ROS) and superoxide dismutase(SOD) were detected by kits. A cisplatin-induced mouse kidney injury model was further established, and the serum urea nitrogen level was detected after the administration of 40 mg·kg^–1 pyridoxine treatment, the results of hematoxylin-eosin staining in renal tissue were analyzed, and the expression of NRF2 was detected by Western blotting.

RESULTS  Pyridoxine could protect kidney injury caused by cisplatin in HK-2 cells and mouse in vivo. In HK-2 cells, pyridoxine down-regulated ROS level, up-regulated SOD enzyme activity, and up-regulated the expression of NRF2 and its downstream antioxidant-related gene HO-1. Pyridoxine significantly reduced the level of serum urea nitrogen, repaired kidney tissue damage, and up-regulated the expression of NRF2 in kidney injury mice.

CONCLUSION  Pyridoxine protects against cisplatin-induced kidney injury through enhancing the level of anti-oxidative stress.