Imidacloprid-induced liver fibrosis in quails via activation of the TGF-β1/Smad pathway

Abstract

Imidacloprid (IMI) is one of the most frequently used neonicotinoid insecticide, and its potential toxicity and environmental hazards have gradually attracted people's attention. Liver fibrosis caused by long-term inflammation or oxidative stress can lead to cirrhosis and liver failure, even death. However, the mechanism of liver fibrosis induced by neonicotinoid insecticide remains unclear. This study investigates whether IMI could induce liver fibrosis in quails and a potential mechanism. Our study used a quail 90-day IMI-induced liver fibrosis model. The results showed that IMI induced histopathological lesions, oxidative stress, inflammation, fibrosis, and changes in nuclear factor-kappa B (NF-κB), nuclear factor-E2-related factor-2 (Nrf2), and transforming growth factor (TGF-β1) levels. Furthermore, IMI enhanced the expression of liver fibrosis marker proteins, including collagen I, α-smooth muscle actin (α-SMA), and fibronectin 1 (FN-1), by activating the TGF-β1/Smad signaling pathway. In conclusion, our study demonstrated that IMI exposure induces liver fibrosis via activation of the TGF-β1/Smad signaling pathway in quails.

Keywords: Imidacloprid; Liver fibrosis; NF-κB; Nrf2; Oxidative stress; TGF-β1/Smad.