title: TOP1 and 2, polysaccharides from Taraxacum officinale, attenuate CCl(4)-induced hepatic damage through the modulation of NF-kappaB and its regulatory mediators.
abstract: In this work, we estimate the inhibitory effect of two polysaccharides from Taraxacum officinale (TOP) on CCl(4)-induced oxidative stress and inflammation in Sprague-Dawley rats. TOP1 and 2 (304, 92 mg/kg bw) were administered for 7 days via a stomach sonde, and hepatitis was induced by a single dose of CCl(4) (50% CCl(4)/olive oil; 0.5 mL/kg bw) administration. CCl(4) significantly elevated serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. Histopathological observation further revealed that CCl(4)-induced moderate levels of inflammatory cell infiltration, centrilobular fatty change, apoptosis, and necrosis. However, TOPs pretreatment markedly decreased AST and ALT activities as well as hepatic lesions. TOPs also increased free radical scavenging activity, as exhibited by a lowered TBARS concentration. TOPs pretreatment also reversed other hepatitis-associated symptoms, including GSH depletion, inhibited anti-oxidative enzyme activities, up-regulation of NF-kappaB and increased expression of its regulatory inflammatory mediators, such as inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1beta. These results suggest that TOPs have a hepatoprotective effect by modulating inflammatory responses and ameliorating oxidative stress.
authors.affiliation: Department of Smart Foods and Drugs, Biohealth Products Research Center, Inje University, Obang-dong 607, Gimhae, Gyeongnam, Republic of Korea.
authors.forename: Chung Mu
authors.initials: CM
authors.lastname: Park
authors.forename: Hyun Joo
authors.initials: HJ
authors.lastname: Youn
authors.forename: Hee Kyung
authors.initials: HK
authors.lastname: Chang
authors.forename: Young Sun
authors.initials: YS
authors.lastname: Song
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D017209:Apoptosis; D001219:Aspartate Aminotransferases / Q000097:blood; D002251:Carbon Tetrachloride / Q000633:toxicity; D002252:Carbon Tetrachloride Poisoning / Q000517:prevention & control; D056486:Chemical and Drug Induced Liver Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009336:Necrosis; D018384:Oxidative Stress / Q000187:drug effects; D010088:Oxidoreductases / Q000037:antagonists & inhibitors / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology; D011134:Polysaccharides / Q000494:pharmacology*; D051381:Rats; D031205:Taraxacum / Q000737:chemistry*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D016166:Free Radical Scavengers; D016328:NF-kappa B; D010936:Plant Extracts; D011134:Polysaccharides; D017392:Thiobarbituric Acid Reactive Substances; D002251:Carbon Tetrachloride; D010088:Oxidoreductases; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione