Inhibition of the Nrf2 signaling pathway involved in imidacloprid-induced liver fibrosis in Coturnix japonica.

Abstract

Imidacloprid (IMI) is a kind of widely used neonicotinoid insecticide. However, the toxicity of IMI is not only applied to target pests but also causes serious negative effects on birds and other creatures. Our previous studies have shown that long-term exposure to IMI can induce liver fibrosis in quails. However, the specific mechanism of quail liver fibrosis induced by IMI is not completely clear. Accordingly, the purpose of this study is to further clarify the potential molecular mechanism of IMI-induced liver fibrosis in quails. Japanese quails (Coturnix japonica) were treated with/without IMI (intragastric administration with 6mg/kg body weight) in the presence/absence of luteolin (Lut) (fed with 800 mg/kg) for 90 days. The results reveal that IMI can induce hepatic fibrosis, oxidative stress, fatty degeneration, inflammation, and the down-expression of nuclear factor-E2-related factor-2 (Nrf2). Furthermore, the treatment of Lut, a kind of Nrf2 activator, increased the expression of Nrf2 in livers and alleviated liver fibrosis in quails. Altogether, our study demonstrates that inhibition of the Nrf2 pathway is the key to liver fibrosis induced by IMI in quails. These results provide a new understanding for the study of the toxicity of IMI and a practical basis for the treatment of liver fibrosis caused by IMI.