Cadmium exposure induced spleen inflammation by activating the MAPK/NF-κB/ NLRP3 signaling pathway and the intervention effect of astilbin.

Abstract

Cadmium (Cd) is an environmental pollutant with strong immunotoxicity effects. Despite this, the mechanisms by which Cd causes spleen damage in chickens are not well understood. Astilbin (ASB) is a dihydroflavone glycoside with anti-inflammatory and anti-oxidation properties. In the present study, a chicken spleen injury model induced by cadmium exposure (90d) was established to explore the specific mechanisms of Cd-induced spleen injury. If and how ASB ameliorates the damage was also explored. A total of 60 chickens were randomly divided into four groups: Con, Cd, ASB, and Cd+ASB groups. The pathological changes in the spleen were observed by H&E staining. Cd-induced oxidative stress, inflammation, and the involvement of the MAPK/NF-κB/NLRP3 in ameliorating spleen damage were also analyzed by Western blotting, qRT-PCR, and immunohistochemistry. Our results showed that Cd exposure for 90 days damaged the spleen, which mainly manifested as eosinophil infiltration, an increase in MDA content, a decrease in the CAT, GSH, SOD, and T-AOC, and activation of MAPK/NF-κB/NLRP3 signaling pathway. The overall outcome of these events was the induction of oxidative stress and inflammation in the spleen of the chickens. Interestingly, ASB treatment ameliorated Cd-induced damages. In conclusion, the present study revealed the specific mechanism of Cd-induced spleen damage using a chicken model. But ASB ameliorates Cd-induced cadmium poisoning.