| Selenium(Se) is one of the essential trace elements in human and animal. Se deficiency can cause a series of diseases. Pancreas is one of the target organs acted by Se deficiency. Pancreatic degeneration, necrosis even fibrosis were the typical pathological changes of chicken with Se deficiency diseases. Previous studies showed that selenoproteins is the main and important way of Se playing the biological effect, and Se also plays a key role in regulating the expression of selenoproteins in vivo. However, the inflammatory injury of pancreas by Se deficiency had not been minutely reported. In this study, the 180 chicken(1 day old) were randomly and equally fed in groups according to the Se level of diet: low-Se group(L group) and control group(C group). L group chicken fed Se deficient(with Se 0.033 mg/kg) diet and C group chicken fed normal(with Se 0.2 mg/kg) diet. We collected pancreas at 15, 25, 35, 45 and 55 d respectively, observing the pathological changes of chicken pancreas, at the same time detecting the mRNA expression level changes of 24 selenoproteins(GPX1, GPX2, GPX3, GPX4, DIOl, DIO2, DIO3, TXNEDl, TXNED2, TXNED3, SEPNl, SEPPl, SELO, SELK, SELS, SELT, SEPX1, SEP15, SELI, SELU, SELH, SELM, SELPB and SPS2), inflammatory factors(i NOSã€COX2ã€PTGEsã€TNF-α and NF-κB) and heat shock proteins(HSPs)(HSP27, HSP40, HSP60, HSP70 and HSP90) and the protein expression level changes of NF-κBã€i NOSã€HSP60ã€HSP70 and HSP90 in chicken pancreas, to explore the regulation effects of Se deficiency on the expression level changes of 24 selenoproteins and the following inflammatory injury. The main results of our study appear below:(1) Se deficiency could cause pathological changes of chicken pancreatic histology and cell ultrastructure, local acinar epithelial cells atrophy, degeneration or loss, peripheral tissue infiltrated with inflammatory cells such as lymphocytes and mononuclear cells, karyopyknosis, chromatin with edge polymerization and membrane performance with a typical apoptosis, endoplasmic reticulum swelling and interstitial thickening, mitochondrial cristae dissolving and vacuolization, and cause inflammatory injury.(2) Se deficiency could significantly reduce the m RNA levels of 24 selenoproteins in chicken pancreas, and selenoproteins including GPX1, GPX3, DIO1, TXNRD1, SEPN1, SEPP1, SELK, SELI, SELM, SEPX1 and SPS2 were obviously effected as a result of Se deficiency, which suggested that Se deficiency can reduce the transcription levels of selenoproteins especially antioxidant selenoproteins.(4) Se deficiency could significantly increase the m RNA levels of inflammatory factors(i NOSã€COX2ã€PTGEsã€TNF-α and NF-κB) and the protein levels of NF-κB and i NOS in chicken pancreas, revealing that Se deficiency induced chicken pancreas inflammatory injury by regulating NF-κB signal pathway.(5) Se deficiency could significantly increase the m RNA levels HSPs and the protein levels of HSP60, HSP70 and HSP90, suggesting HSPs involved the process of inflammatory injury by Se deficiency. |