Inhibitory effect of MIL glycoprotein on expression of pro-inflammatory mediators in carbon tetrachloride-induced mice liver damage.
The aim of the present study was to evaluate immunomodulatory and hepatoprotective effects of glycoprotein isolated from Morus indica Linne (MIL glycoprotein) on carbon tetrachloride (CCl(4) )-induced liver injury. In the present study, MIL glycoprotein (5 and 10 mg kg(-1) body weight) was administered to ICR mice for 7 days prior to CCl(4) treatment. We evaluated the activities of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and thiobarbituric acid-reactive substances (TBARS), and expression of inflammation-related mediators including cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α, and interleukin (IL)-1 beta in CCl(4) -treated mice. Our results revealed that MIL glycoprotein reduced the activities of ALT, LDH and TBARS in serum from CCl(4) -treated mice. We also found that MIL glycoprotein reduced the activity of COX-2 and expression of TNF-α and IL-1 beta in liver from CCl(4) -treated mice. Moreover, administration of MIL glycoprotein suppressed on stress-activated protein kinase/c-jun N-terminal kinase phosphorylation and activator protein-1 transcriptional activation in livers from CCl(4) -treated mice. The results from these experiments indicate that MIL glycoprotein effectively protects against liver injury, mainly through downregulation of oxidative stress and the inflammatory response. In conclusion, we suggest that the MIL glycoprotein might be one component of health supplements for prevention of liver diseases.
Oh
Phil-Sun
PS
Molecular Biochemistry Laboratory, Biotechnology Research Institute and Center for the Control of Animal Hazards Using Biotechnology (BK21), Chonnam National University, 300 Yongbong-Dong, Gwang-ju 500-757, South Korea.
Lee
Jin
J
Lim
Kye-Taek
KT
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D002251:Carbon Tetrachloride / Q000633:toxicity*; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism / Q000517:prevention & control; D056486:Chemical and Drug Induced Liver Injury / Q000517:prevention & control*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D006023:Glycoproteins / Q000378:metabolism / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D008099:Liver / Q000187:drug effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D031625:Morus / Q000737:chemistry; D018384:Oxidative Stress; D010940:Plant Proteins / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D006023:Glycoproteins; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D010940:Plant Proteins; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D002251:Carbon Tetrachloride; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D000410:Alanine Transaminase