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Selenium is an essential trace elements of human and animal, plays an important role in the maintenance of many species, including humans, the normal physiological function, and the occurrence of a number of diseases such as Keshan disease, white muscle disease is closely related to liver necrosis and livestock, poultry growth and development, reproduction, immune function and resistance to disease plays an important biological function. The liver is an important accumulation of selenium and selenium poisoning attacks organs, selenium deficiency can be caused by degeneration and necrosis of the liver cell apoptosis, excess selenium can cause selenium poisoning. Animals selenium exists mainly in the form of selenoproteins, selenium exerts its biological effects mainly through selenoproteins. The study found that the amount of selenium intake is associated with some changes in selenoproteins, selenium to a certain extent regulate the expression of selenoproteins. Selenoprotein W is an important member of the family of animals selenoproteins, selenoprotein W mainly in mammals, chicken liver cell apoptosis induced expression and regulation in the the poultry liver tissue within the study has yet reported low selenium The mechanism also few studies. This test Embryonic Chickens and bred cock as experimental subjects. Experimental animals processing as follows, ① The zero-day old chick embryos were divided into 3 groups, wherein the Se-I group, Se-II injection the Na2SeO3 make albumen selenium content of the final concentration to 0.08μg/ml, 0.10μg/ml, respectively, and 12 d, 15 d, 18 d, 21 d sectional chick embryo liver tissue; ② The day-old chicks then divided into three groups, L group, M group and H group were fed fed selenium 0.033 mg / kg, 0.15 mg / kg and 1.5 mg / kg of ration, 15 d, 25 d, 35 d, 45 d and 55 d were killed and mining liver tissue; ③ The day-old rooster then divided into five groups, the Control group was fed the basal diet Se-I, Se-II, Se-III, Se-IV group added Na2SeO3 the selenium content of 0.6 mg / kg, 1.1 mg / kg, 1.5 mg / kg, 2.0 mg / kg were fed killed 90 d take liver tissue. Detection the the liver tissue SelW, SecS, SPS-1 mRNA expression, and group L and M group liver tissue microstructure observation and apoptosis and apoptosis related genes (Caspase-3, Caspase-8, Fas), explore selenium deficiency mechanism and diet of chicken liver cell apoptosis caused by different selenium levels on chicken liver tissue SelW its anabolic enzyme expression, and the results are as follows. Pathological structures observed on chicken liver description fed normal and morphological integrity of the selenium-enriched feed chicken liver, hepatic cords neat rules, no significant changes in organizations. Selenium deficiency can lead to structural abnormalities of liver tissue, hepatic cord disarranged, inflammatory cell infiltration, liver cell degeneration, necrosis and apoptosis. 2 the the selenium content and SelW, SecS, the SPS-1 mRNA in the the rooster liver tissue in chicken embryos, chicks and bred level detection that dietary selenium content in the range of 0.033 mg/kg-2.0 mg / kg, the regulation of liver SelW, SecS, SPS-1 mRNA expression levels were dose-response relationship, chick embryo the liver tissue SelW mRNA expression level was also found dose-response relationship, while SecS, SPS-1 mRNA expression level was fluctuated. 3 chicken liver tissue apoptosis and apoptotic gene caspase-3, Caspase-8, Fas mRNA level of detection, suggesting that selenium deficiency can cause liver tissue apoptosis, Caspase-3, Caspase-8, Fas mRNA expression levels, prompt Fas / Fasl mediated caspase family cascade reaction resulting apoptosis may play an important role in the development process selenium deficiency induced liver injury.
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