High Levels of Boron Exposure Aggravated Hepatocytes Damage in Broilers via Pyroptosis
We aim to explore the mechanism of boron-induced hepatocytes damage in broilers.Thirty AA broiler chickens were randomly divided into control group(CG),low boron group(LBG)and high boron group(HBG).They were fed with different additional doses of boron in the basal diet:the basal diet(boron 0 mg·kg-1),low boron diet(boron 120 mg·kg-1)and high boron diet(boron 240 mg·kg-1),respectively.Liver tissues were collected 7 and 14 days after treatment.The content of boron in liver tissue was determined by ICP-MS,the ASL and ALT levels were tested by automatic blood biochemistry analyzer,the pathological changes in liv-er tissue were observed by H&E staining,ultrastructural changes in liver tissue were observed by transmission electron microscopy,and the localized expressions of NLRP3 and IL-1 β in liver tissue were detected by immunohistochemistry and immunofluorescence.The mRNA and protein expression levels of NLRP3,Casapse-1,IL-1β,IL-18,and GSDMD were detected by RT-qPCR and Western blot.The results showed that the amount of boron stored in the liver tissue as along dietary boron levels increased,with the duration and dosage of exposure.In addition,the struc-tural integrity of the liver tissue of 14-day-low boron group(14 d-LBG)and 14-day-high boron group(14 d-HBG)was significantly compromised,with an increase in pyroptosis levels with an increase in boron dosage.Compared with CG at the same time,a significant upregulation of mR-NA expression levels of NLRP3,Caspase-1 and IL-18 was observed in the 14 d-LBG(P＜0.05).Furthermore,a significant upregulation of both mRNA and protein expression levels of NLRP3,Caspase-1,IL-1β,IL-18 and GSDMD was observed in the 14 d-HBG(P＜0.05).High levels of boron exposure could induce hepatocytes damage in broilers through the pyroptosis pathway.
万方数据
维普
