Protective role of apigenin in cisplatin-induced renal injury

Eur J Pharmacol. 2016 Oct 15:789:215-221. doi: 10.1016/j.ejphar.2016.07.003. Epub 2016 Jul 5.

Abstract

This study aimed to investigate the effects and molecular mechanisms of the effects of apigenin on cisplatin (CP)-induced kidney injury in mice. Apigenin was intraperitoneally administered for 3 consecutive days before CP treatment. We found that apigenin pretreatment significantly attenuated the damage to the kidneys and decreased the levels of serum creatinine, blood urea nitrogen (BUN), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD), which were increased by CP. Apigenin significantly decreased the levels of TNF-α, IL-1β and TGFβ in the kidneys. Additionally, apigenin inhibited the activations of CYP2E1, phospho-NF-κB p65 and phospho-P38 MAPK in CP-induced renal injury. These results suggest that the renoprotective effects of apigenin may be related to the suppressions of oxidative stress and inflammation in CP-induced renal injury in mice.

Keywords: Apigenin; Cisplatin; Inflammation; Kidney; Oxidative stress.

MeSH terms

  • Animals
  • Apigenin / pharmacology*
  • Cisplatin / adverse effects*
  • Cytoprotection / drug effects*
  • Kidney / cytology
  • Kidney / drug effects*
  • Kidney / injuries*
  • Kidney / metabolism
  • Male
  • Mice
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism
  • Transcription Factor RelA / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Reactive Oxygen Species
  • Transcription Factor RelA
  • Apigenin
  • p38 Mitogen-Activated Protein Kinases
  • Cisplatin