Dietary luteolin protects against HgCl2-induced renal injury via activation of Nrf2-mediated signaling in rat

Luteolin (Lut) belongs to the flavonoid family with various beneficial bioactivities. Here, we investigated whether Lut attenuate mercuric chloride (HgCl2)-induced renal injury in rat. We found that oral gavage administration of Lut (80mg/kg) alleviated anemia and renal histology upon HgCl2 treatment (80mg/L). Lut also significantly reduced HgCl2-induced oxidative stress and inflammatory, presenting as the reduced malondialdehyde (MDA) formation, increased glutathione (GSH) level, and inhibited activation of nuclear factor kappa B (NF-κB). Moreover, Lut protected renal cells from HgCl2-induced apoptosis, as assessed by Terminal deoxynucleotidyl transferase dUNT nick end labeling (TUNEL) assay and the protein levels of B-cell lymphoma gene 2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xL), Bcl-2-associated X protein (Bax), and p53. Interestingly, Lut reduced renal mercuric accumulation in rat. Furthermore, Lut increased nuclear translocation of the nuclear factor-erythroid-2-related factor 2 (Nrf2), and subsequent protein expression of the antioxidant enzymes, heme oxygenase-1 (HO-1) and nicotinamide adenine dinucleotide phosphatase: quinone-acceptor 1 (NQO1). Our results suggest that Lut suppress HgCl2-induced renal injury via activation of Nrf2 signaling pathway. Potential mechanism of luteolin in HgCl2-induced renal injury. Luteolin protected against HgCl2-induced renal injury by alleviating oxidative stress and inflammation through regulating the nuclear factor-erythroid-2-related factor 2 (Nrf2)/nuclear factor kappa B (NF-κB) signaling pathway and inhibiting apoptosis by regulating B-cell lymphoma gene 2 (Bcl-2) family proteins expression. [Display omitted] •Oxidative stress is involved in HgCl2-induced renal injury.•Dietary luteolin reduced renal mercuric accumulation.•Dietary luteolin promoted mercuric excretion in the urine.