Luteolin-mediated PI3K/AKT/Nrf2 signaling pathway ameliorates inorganic mercury-induced cardiac injury.

Inorganic mercury is a toxic metal of worldwide concern, and causes serious cardiac injury. However, effective treatment for cardiac injury induced by mercuric chloride (HgCl2) has not been fully identified. Luteolin (Lut) is a novel natural antioxidant. This study aimed to investigate the role of Lut on HgCl2-induced cardiac injury. Male Wistar rats were randomly assigned to 4 groups, control, Lut (80 mg/kg intragastrically), HgCl2 (80 mg/L, in drinking water), and HgCl2 + Lut groups. The results indicated that Lut significantly ameliorated cardiac histopathological damage, oxidative stress, and apoptosis induced by HgCl2 in the rat heart. Furthermore, Lut evidently increased levels of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and nuclear factor-erythroid-2-related factor 2 (Nrf2) and its downstream proteins, and inhibited NF-κB activation in the heart of rats treated by HgCl2. Taken together, our findings suggest that activating PI3K/AKT/Nrf2 signaling pathway is involved in the protective effect of Lut against HgCl2-induced cardiac damage.