HSP27–HSP40–HSP70–HSP90 pathway participated in molecular mechanism of selenium alleviating lead-caused oxidative damage and proteotoxicity in chicken Bursa of Fabricius

Abstract

Lead (Pb), a toxic environmental pollutant, is hazardous to the health of humans and birds. Bursa of Fabricius (BF) is a unique organ of birds. Toxic substances can attack BF and induce proteotoxicity. Increased heat shock proteins (HSPs) can induce oxidative damage. Selenium (Se) can alleviate harmful substance-caused oxidative damage. This study aimed to investigate whether Pb can cause oxidative damage and proteotoxicity, as well as Se reverse Pb-caused chicken BF toxicity. A model of chickens treated with Se and Pb alone and in combination was established. BFs were collected on days 30, 60, and 90. H&E and qRT-PCR were performed to observe the microstructure and to detect HSP27, HSP40, HSP60, HSP70, and HSP90 mRNA levels, respectively, in BFs. Multivariate correlation analysis and principal component analysis were conducted to explore the correlation among the five HSPs. In our results, Pb caused BF damage and up-regulated the five HSPs at three time points, causing oxidative damage and proteotoxicity via HSP27–HSP40–HSP70–HSP90 pathway. Furthermore, Pb caused time-dependent stress on HSP27, HSP40, HSP60, and HSP70. In addition, Se relieved Pb-caused damage and up-regulation of HSPs. Taken together, we concluded that Se alleviated Pb-caused oxidative injury and proteotoxicity in chicken BFs via the HSP27–HSP40–HSP70–HSP90 pathway.