title: Sesamin reduces acute hepatic injury induced by lead coupled with lipopolysaccharide.
abstract: BACKGROUND
  In this study, we investigated the potential anti-inflammatory and antioxidative effects of sesamin on acute liver injury. Lead (Pb) causes oxidative damage and enhances the effects of low-dose lipopolysaccharide (LPS), inducing acute hepatic injury in rats.
  
  
  METHODS
  Male Sprague-Dawley rats were given intraperitoneal injections of Pb acetate (5 mg/kg) and LPS (50 μg/kg) to induce liver injury, and we tested the effects of oral administration of sesamin (10 mg/kg) on liver damage. To assess the extent of acute hepatic injury in the rats, we measured the anti-inflammatory and antioxidant markers and relevant signaling pathways: serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), C-reactive protein (CRP), reactive oxygen species (ROS), tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, nitric oxide (NO), and cyclooxygenase-2 (COX-2), inducible NO synthase (iNOS) levels, mitogen-activated protein kinases (MAPKs), c-Fos, and GADD45β.
  
  
  RESULTS
  Sesamin significantly decreased the serum AST, ALT, and CRP levels in the rat model. In the Pb and LPS-stressed rats, sesamin administration reduced the serum levels of TNF-α, IL-1, IL-6, NO, and ROS generation, and liver tissue expressions of c-Jun N-terminal kinase (JNK), p38 MAPK, GADD45β, COX-2, and iNOS.
  
  
  CONCLUSIONS
  Collectively, these results demonstrate that sesamin is associated with antioxidant and anti-inflammatory activity. The observed effect of scavenging of ROS and NO and inhibiting the production of proinflammatory cytokines may be achieved through the suppression of COX-2, iNOS, and MAPK pathways in the acute hepatic injury rats.
authors.affiliation: Department of Cosmeceutics, China Medical University, Taichung, Taiwan, ROC.
authors.forename: Hsiu-Mei
authors.initials: HM
authors.lastname: Chiang
authors.affiliation: Department of Biotechnology, Yuanpei University, Hsinchu, Taiwan, ROC.
authors.forename: Hsiang
authors.initials: H
authors.lastname: Chang
authors.affiliation: Institute of Biotechnology, National TsingHua University, Hsinchu, Taiwan, ROC.
authors.forename: Pei-Wun
authors.initials: PW
authors.lastname: Yao
authors.affiliation: Department of Food Nutrition, Hungkuang University, Taichung, Taiwan, ROC.
authors.forename: Yuh-Shuen
authors.initials: YS
authors.lastname: Chen
authors.affiliation: Department of Medical Research, Tungs' Taichung MetroHarbor Hospital, Taichung, Taiwan, ROC.
authors.forename: Kee-Ching
authors.initials: KC
authors.lastname: Jeng
authors.affiliation: Department of Chinese Medicine, Taichung Tzuchi Hospital, Taichung, Taiwan, ROC.
authors.forename: Jen-Shu
authors.initials: JS
authors.lastname: Wang
authors.affiliation: Department of Biotechnology, Yuanpei University, Hsinchu, Taiwan, ROC. Electronic address: rolis.hou@mail.ypu.edu.tw.
authors.forename: Chien-Wei
authors.initials: CW
authors.lastname: Hou
mesh_terms: D000208:Acute Disease; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy*; D004149:Dioxoles / Q000627:therapeutic use*; D017705:Lignans / Q000627:therapeutic use*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D009942:Organometallic Compounds / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D004149:Dioxoles; D017705:Lignans; D008070:Lipopolysaccharides; D009942:Organometallic Compounds; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C008261:lead acetate; C054125:sesamin
keywords: cyclooxygenase-2; inducible nitric oxide synthase; kinases; mitogen-activated protein; sesamin