Evodiamine attenuates cadmium-induced nephrotoxicity through activation of Nrf2/HO-1 pathway

Purpose: To investigate the protective role of evodiamine, a naturally occurring anti-inflammatory, antioxidant, and anti-apoptotic compound, against cadmium-induced cytotoxicity in proximal tubular cells (human kidney 2; HK-2).
 Methods: HK-2 were treated with different concentrations evodiamine (5, 20, 50 ?M) for 2 h then incubated 40 ?M cadmium chloride another 24 h. Cell viability apoptosis evaluated using thiazolyl blue tetrazolium bromide (MTT) flow cytometry, respectively. Oxidative stress was assayed by measuring levels malonaldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) peroxidase (GSH-PX).
 Results: Cadmium treatment significantly reduced cell (p < 0.01) increased compared to control. Evodiamine pretreatment attenuated chloride-provoked decrease increase apoptosis. also decreased expression cleaved caspase-3 caspase-9 cells. exposure provoked injury, as evidenced MDA SOD, GSH, GSH-PX levels. Pretreatment ameliorated shown expression. enhanced protein nuclear factor erythropoietin-2-related (Nrf2) heme oxygenase 1 (HO-1).
 Conclusion: exerts an anti-oxidative effect chloride-induced nephrotoxicity via Nrf2/HO-1 pathway activation. These findings represent potential therapeutic strategy cadmium-provoked nephrotoxicity.