Protective Action of Se-Supplement Against Acute Alcoholism Is Regulated by Selenoprotein P (SelP) in the Liver
- 528 Downloads
Acute alcoholism is a major cause of cirrhosis and liver failure around the world. Selenium (Se) is an essential micronutrient promoting liver health in humans and animals. Selenoprotein P (SelP) is a glycoprotein secreted within the liver, which interacts with cytokines and the growth factor pathway to provide protection for hepatic cells. The present study was conducted to confirm the effect and mechanism of Se and SelP action in livers affected by acute alcoholism. In this study, a mouse model of acute alcoholism, as well as a hepatocyte model, was successfully established. The Se content of the liver was detected by atomic fluorescence spectrophotometry. The expression of messenger RNA (mRNA) was analyzed by quantitative polymerase chain reaction (qPCR). The protein expression of inflammatory factors was detected by ELISA. The other proteins were analyzed by western blotting. The results showed that pathological damage to the liver was gradually weakened by Se-supplementation, which was evaluated by hematoxylin and eosin (H&E) and TUNEL staining. Se-supplementation inhibited expression of pro-inflammatory factors TNF-α and IL-1β and promoted production of anti-inflammatory cytokine IL-10 in the liver with acute alcoholism. Se-supplementation also prevented the apoptosis of hepatocytes by suppressing the cleavage of caspases-9, 3, 6, 7, and poly(ADP-ribose) polymerase (PARP). Through correlational analysis, it was determined that the effects of Se-supplement were closely related to SelP expression, inflammatory cytokines, and apoptosis molecule production. The sienna of SelP further confirmed the protective action of Se-supplementation on the liver and that the mechanism of SelP involves the regulation of inflammatory cytokines and apoptosis molecules in acute alcoholism. These findings provide information regarding a new potential target for the treatment of acute alcoholism.
KeywordsSelenium (Se) Selenoprotein P (SelP) Acute alcoholism Liver Protective
This work was supported by a grant from the Fundamental Research Funds for the Central Universities (No. 2662014BQ024), the National Natural Science Foundation of China (Nos. 31502130, 31472254, and 31272631), and Undergraduate Special Science and Technology Innovation of Huazhong Agricultural University (No. 2015BC009).
- 3.Thursz M, Morgan TR (2016) Treatment of severe alcoholic hepatitis. Gastroenterology 150:1823–34Google Scholar
- 7.Ju C, Mandrekar P (2015) Macrophages and alcohol-related liver inflammation. Alcohol Res Curr Rev 37:251–262Google Scholar
- 17.Nourbakhsh M, Ahmadpour F, Chahardoli B, Malekpour-Dehkordi Z, Nourbakhsh M, Hosseini-Fard SR, et al. (2016) Selenium and its relationship with selenoprotein P and glutathione peroxidase in children and adolescents with Hashimoto’s thyroiditis and hypothyroidism. J Trace Elem Med Biol: Organ Soc Miner Trace Elem 34:10–14CrossRefGoogle Scholar
- 30.Chan DS, Wong M (1997) Multidisciplinary handbook on pediatric nutritional support. Am J Health Syst Pharm: AJHP: Off J Am Soc Health Syst Pharm 54:1355Google Scholar
- 31.Liu Y, Qiu C, Li W, Mu W, Li C, Guo M (2016) Selenium plays a protective role in staphylococcus aureus-induced endometritis in the uterine tissue of rats. Biol Trace Elem Res:1–9Google Scholar
- 43.Into T, Shibata K (2005) Apoptosis signal-regulating kinase 1-mediated sustained p38 mitogen-activated protein kinase activation regulates mycoplasmal lipoprotein- and staphylococcal peptidoglycan-triggered toll-like receptor 2 signalling pathways. Cell Microbiol 7:1305–1317CrossRefPubMedGoogle Scholar
- 48.Burk RF, Hill KE, Read R, Bellew T (1991) Response of rat selenoprotein P to selenium administration and fate of its selenium. Am J Phys 261:E26–E30Google Scholar