title: [Research of Herba Artemisiae Scoporiae inhibits the hepatic lipotoxicity].
abstract: OBJECTIVE
  To study the efficiency and effect mechanism of Herba Artemisiae Scoporiae inhibits the hepatic lipotoxicity model in vitro.
  
  
  METHODS
  Preparation rat regular serum and medicine serum. Under the safty of medicine thickness by toxicity testing, normal and model groups were added 10% normal rat serum, Herba Artemisiae Scoporiae group was added 10% medicine serum incubation for 24 h, FFA was added to all the groups but the normal incubation for 24 h. The indices were tested below: the content of serum tumor necrosis factor alpha (TNF-alpha) by ELISA, cellular triglyceride content (TG), Oil Red Staining; protein expression of cellular Bcl-2 Assaciated X protein (Bax), phospho-IKB (P-IkappaB) and Cathepsin B (ctsb) by Western Blotting; gene expression of cellular TNF-alpha, Bax and ctsb by real-time PCR; the expression and distribution of ctsb observed by immunofluorescence.
  
  
  RESULTS
  After being incubated with FFA for 24 hours, TG deposition of HepG2 in the model group increased markedly. Compared with normal group, not only the content of serum TNF-alpha, but also the protein expression of cellular ctsb, P-IkappaB and mRNA expression of ctsb, TNF-a increased significantly. Contrast to model group, TG deposition decreased markedly in the Herba Artemisiae Scoporiae group. The Herba Artemisiae Scoporiae inhibited TNF-alpha content, the protein expression of cellular ctsb, P-IkappaB and mRNA expression of TNF-alpha significantly.
  
  
  CONCLUSIONS
  Herba Artemisiae Scoporiae has a direct inhibition on HepG2 steatosis and TNF-alpha secretion induced by long-chain FFA. The effect mechanism of Herba Artemisiae Scoporiae inhibits the hepatic lipotoxicity has close relationship with inhibition on the protein expression and mRNA expression of ctsb.
authors.affiliation: Institute of Liver Diseases of Shuguang Hospital, Key Laboratory for Liver-kidney Disease Pattern of Ministry of Education, E-Institute of Shanghai Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. csd5035201@yahoo.com.cn
authors.forename: Shaodong
authors.initials: S
authors.lastname: Chen
authors.forename: Qin
authors.initials: Q
authors.lastname: Feng
authors.forename: Jinhua
authors.initials: J
authors.lastname: Peng
authors.forename: Lili
authors.initials: L
authors.lastname: Xu
authors.forename: Ping
authors.initials: P
authors.lastname: Liu
authors.forename: Cheng
authors.initials: C
authors.lastname: Liu
authors.forename: Yiyang
authors.initials: Y
authors.lastname: Hu
mesh_terms: D000818:Animals; D019306:Artemisia / Q000737:chemistry*; D015536:Down-Regulation / Q000187:drug effects*; D005230:Fatty Acids, Nonesterified / Q000633:toxicity*; D015870:Gene Expression / Q000187:drug effects; D056945:Hep G2 Cells; D006801:Humans; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D005230:Fatty Acids, Nonesterified; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha