Lipids in Health and Disease | |
Activation of peroxisome proliferator activated receptor alpha ameliorates ethanol induced steatohepatitis in mice | |
Research | |
Yuemin Nan1  Lingbo Kong1  Weiguang Ren1  Wenjuan Wu1  Yuguo Zhang1  Suxian Zhao1  Wencong Li1  Rongqi Wang1  Hongmei Mi1  Jun Yu2  | |
[1] Department of Traditional and Western Medical Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang, China;Institute of Digestive Disease and Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong; | |
关键词: Peroxisome proliferator activated receptor alpha; ethanol; steatohepatitis; animal experiment; | |
DOI : 10.1186/1476-511X-10-246 | |
received in 2011-11-19, accepted in 2011-12-30, 发布年份 2011 | |
来源: Springer | |
【 摘 要 】
BackgroundPeroxisome proliferator activated receptor alpha (PPARα) regulates lipids metabolism and inhibits inflammatory response. However, the role of PPARα in alcoholic liver disease is largely unknown. We aim to elucidate the effect and the molecular basis of PPARα in ethanol induced hepatic injury in mice.ResultsC57BL/6J mice fed with 4% ethanol-containing Lieber-DeCarli liquid diet for 12 weeks exhibited hepatocyte steatosis, necrosis and inflammatory infiltration, accompanied with elevated serum alanine aminotransferase (ALT) and aspartic transaminase (AST) levels, decreased hepatic expression of PPARα, lipids oxidation promoting genes and anti-inflammatory factors, as well as enhanced hepatic expression of fatty acids synthesis promoting genes and pro-inflammatory cytokines. Induction of PPARα by PPARα agonist WY14643 treatment for 2 weeks ameliorated the severity of liver injury and restored expression of genes altered by ethanol treatment. However, administration of PPARα antagonist GW6471 for 2 weeks promoted the inflammatory response.ConclusionsThe present study provided the evidence for the protective role of PPARα in ameliorating ethanol induced liver injury through modulation of the genes related to lipid metabolism and inflammatory response.
【 授权许可】
Unknown
© Kong et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
【 预 览 】
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