Lycium barbarum polysaccharide alleviate cadmium-induced mitochondrial dysfunction mediated pyroptosis in duck liver

Cadmium (Cd) is a persistent environmental heavy metal pollutant that has been an important issue in toxicology research worldwide. This toxic element is non-degradable and accumulates indefinitely in the ecosystem, and gradually accumulates in living organisms through nutrient transfer, ultimately posing a significant risk to the health of animals. The hepatic system is both the main target organ for Cd bioaccumulation and the metabolic center of organisms, and is particularly susceptible to heavy metal exposure. However, the underlying mechanism of whether LBP protects against Cd-induced liver injury in male Shaoxing ducks is still unknown. In our study, male Shaoxing ducks were treated with Cdcl₂ (50 mg/kg) and/or LBP (50 mg/kg) for 30 days. We found that Cd exposure reduced the growth rate, feed intake, liver weight and organ index, and increased the serum biochemical indexes (AST, ALT, ALP) in Shaoxing ducks. Further studies have shown that Cd induces liver pathological damage and macro/trace element metabolism disorders, thereby inhibiting the activity of Nrf2 antioxidant signaling pathway and further inducing oxidative stress. Finally, we found that Cd induces the destruction of liver mitochondrial structure, disrupts the normal mitochondrial biogenesis and fusion/fission disorder, and thus causes liver pyroptosis and fibrosis. In this process, we found that LBP administration significantly improved Cd-induced growth inhibition and liver damage.