Nano-Selenium Antagonized Cadmium-Induced Liver Fibrosis in Chicken

Cadmium is a global ecological toxic pollutant; in animals, hepatotoxic fibrosis is caused by bioaccumulation of Cd through food chains. We determined the path of nano-Se antagonism in Cd-induced hepatocyte pyroptosis by targeting the APJAMPK-PGC1 alpha pathway, using an in vivo model of hepatotoxicity. All 1-day-old chicks were treated with Cd (140 mg/kg BW/day) and/or nano-Se (0.3 or 0.6 mg/kg BW/day) for 90 days. The result showed that Cd (1.55 +/- 0.148) activated NLRP3 inflammasome 49.903% as compared to the Con group (1.034 +/- 0.008) to release the inflammasome as a result of hepatocyte pyroptosis (2.824 +/- 0.057). Compared with the Con group (1.010 +/- 0.021), Kupffer cells were 219.109% more to activate astrocytes through the APJAMPK-PGC1 alpha pathway, resulting in 185.149% more hepatic fibrosis. However, the fibrosis degree of the H-Se + Cd group (1.252 +/- 0.056) was 56.5278% (p < 0.001) lower than that of the Cd group (2.880 +/- 0.124). Therefore, this study established that pyroptotic hepatocytes and Kupffer cells could be targeted for nano-Se antagonizing Cd toxicity, which reveals a potential new approach targeting astrocytes for the treatment of liver fibrosis triggered by Cd pollution.

Automated summary

This study determined the mechanism of nano-Se antagonism in Cd-induced hepatocyte pyroptosis by targeting the APJAMPK-PGC1 alpha pathway. The results showed that Cd activated the NLRP3 inflammasome and caused hepatocyte pyroptosis. Furthermore, Cd also increased hepatic fibrosis. However, the co-treatment of nano-Se and Cd significantly reduced the degree of fibrosis.