title: Melatonin-selenium nanoparticles protects liver against immunological injury induced by bacillus Calmette-Guerin and lipopolysaccharide.
abstract: OBJECTIVE
  Melatonin-selenium nanoparticle (MT-Se), a novel complex, was synthesized by preparing selenium nanoparticles in a melatonin medium. The present investigation was designed to determine the protective effects of MT-Se against immunological liver injury in mice induced by bacillus Calmette-Guerin (BCG)/lipopolysaccharide (LPS).
  
  
  METHODS
  The model of immunological liver injury in mice was prepared. The levels of alanine aminotransferase, aspartate amino-transferase, nitric oxide (NO) in serum, malondialdehyde content, superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) activities in a liver homogenate were assayed by spectrophotometry. The content of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) were determined by ELISA. The splenocyte proliferation was assayed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) dye reduction. Meanwhile, a hepatic pathological examination was observed.
  
  
  RESULTS
  In the BCG/LPS-induced hepatic injury model, MT-Se administered at doses of 5, 10, or 20 mg/kg to the BCG/LPS-treated mice for 10 d significantly reduced the increase in serum aminotransferase, reduced the severe extent of hepatic cell damage and the immigration of inflammatory cells. It also attenuated the increase in the content of thiobarbituric acid-reactive substances and enhanced the decrease in activities of SOD and GSH-px. In contrast, the treatment with MT-Se suppressed the increase in NO level in both the serum and liver tissue. Furthermore, MT-Se significantly lowered an increase in TNF-alpha and IL-1beta levels in the liver and inhibited the production of TNF- alpha and IL-1beta by peritoneal macrophages. A downregulation effect of MT-Se on splenocyte proliferation was also observed.
  
  
  CONCLUSIONS
  MT-Se showed a hepatic protective action on immunological liver injury in mice.
authors.affiliation: Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, China.
authors.forename: Hua
authors.initials: H
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Wei
authors.forename: Sheng-yi
authors.initials: SY
authors.lastname: Zhang
authors.forename: Yu-xian
authors.initials: YX
authors.lastname: Shen
authors.forename: Ni-ping
authors.initials: NP
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Yue
authors.forename: Shu-yun
authors.initials: SY
authors.lastname: Xu
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D005979:Glutathione Peroxidase / Q000378:metabolism; D006520:Hepatitis, Animal / Q000139:chemically induced / Q000378:metabolism; D007375:Interleukin-1 / Q000096:biosynthesis / Q000378:metabolism; D008070:Lipopolysaccharides; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D017737:Macrophages, Peritoneal / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008550:Melatonin / Q000494:pharmacology*; D051379:Mice; D009163:Mycobacterium bovis; D049329:Nanostructures; D009569:Nitric Oxide / Q000097:blood / Q000378:metabolism; D012643:Selenium / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D000637:Transaminases / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000637:Transaminases; D000410:Alanine Transaminase; D012643:Selenium; D008550:Melatonin