Effect Of Selenium Deficiency On Inflammatory Cytokine And Heat Shock Protein Expressions In Chicken Aorta Vessels

Selenium(Se) is an essential micronutrient for body, and exists in various organs and body fluids, which participates in many physiological and biochemical activities. Se deficiency can cause a variety of diseases, such as cardiovascular disease, cancer, and liver disease. Se plays an important role in the body’s antioxidant processes by constituting the active center of variety of antioxidant enzymes. The biological functions of Se are mainly elicited through selenoprotein proteins. Se can regulate the expression levels and activity of selenoproteins, Se deficiency is linked with inflammation which could cause cardiovascular disease, and Se can enhance the function of immune cells, therefore it is considered as an anti-inflammatory agent. Currently, the biological function of selenium is well studied, and the effects of Se deficiency on the various organs have been reported, but there is little studies about vascular injury caused by Se deficiency. Vascular disease could lead to the development of cardiovascular disease directly or indirectly. This study investigated the effect of dietary Se deficiency on chicken aorta vessels injury, which would provide important theoretical basis for the study of selenium.180 one-day-old chicks were randomly divided into two groups, control group(C group) and low-Se group(L group). The chickens in L group was fed a basal Se-deficient diet(0.033 mg/kg Se); and the C group was fed a diet identical to that of the L group, but supplemented sodium selenite to make the final Se content 0.2 mg/kg. Then aortas were collected at 15 d, 25 d, 35 d, 45 d, 55 d, and 65 d. By detecting the antioxidant function and expression levels of selenoproteins, inflammatory cytokines(including NF-κB, TNF-α, PGTE, COX-2 and i NOS), and heat shock protein(including Hsp27, Hsp40, Hsp60, Hsp70 and Hsp90), we investigate the effect of Se deficiency on aorta vessels injury. The mains results were showed as follows:(1) Compared with C group, chicken in L group got typical clinical symptom caused by Se decifiency, and Ultrastructure changed. The results indicated that Se deficiency model replicated successfully, and arterial injury was caused by selenium deficiency.(2) Dietary Se deficiency could make a decrease in GSH content, Gpx and CAT activity, and an increase in i NOS activity, MDA and NO content. The results indicated that oxidative stress participated in the process of arterial injury caused by selenium deficiency.(3) Se deficiency could significantly decrease the expression levels of 25 selenoproteins, except Gpx4, which only had an significant decrease in mRNA expression levels at 45 d.(4) Se deficiency could significantly increase the expressions of inflammatory factors in chicken aorta, NF-κB, TNF-α, COX-2, PTGEs and i NOS m RNA expression levels were significantly increased, increased significantly. It was suggested that inflammatory factors participated in the process of arterial injury caused by selenium deficiency.(5) Se deficiency could significantly increase the expressions of heat shock proteins in chicken aorta, Hsp27, Hsp40, Hsp60, Hsp70 and Hsp90 m RNA expression levels were significantly increased, and protein expression levels of Hsp60, Hsp70 and Hsp90 were also increased significantly. It was suggested that heat shock proteins participated in the process of arterial injury caused by selenium deficiency.