title: Berberine inhibits dyslipidemia in C57BL/6 mice with lipopolysaccharide induced inflammation.
abstract: BACKGROUND
  Inhibiting the action of proprotein convertase subtilisin/kexin type 9 (PCSK9) on the low-density lipoprotein receptor (LDLR) has emerged as a novel therapeutic target for hypercholesterolemia. Here we investigated the effect of berberine, natural plant extracts, on PCSK9-LDLR pathway in C57BL/6 mice with lipopolysaccharide (LPS) induced inflammation.
  
  
  METHODS
  Forty female mice were divided into four groups (n =10): control, LPS (5 mg/kg), LPS + berberine 10 (5 mg/kg LPS plus 10 mg/kg berberine), and LPS + berberine 30 (5 mg/kg LPS plus 30 mg/kg berberine). Changes in the levels of blood lipids [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)]; pro-inflammatory cytokines [interferon-γ (IFNγ), tumor necrosis factor α (TNFα), and interleukin-1α (IL-1α)], 8-isoprostane, hepatic expressions of PCSK9 and LDLR were determined.
  
  
  RESULTS
  Berberine pretreatment reduced the expression of hepatic PCSK9, decreased the plasma TC, TG, LDL-C, IFNγ, TNFα, IL-1α, and 8-isoprostane concentrations; increased HDL-C level and LDLR expression in mice.
  
  
  CONCLUSIONS
  The present results suggest that berberine inhibits dyslipidemia in C57BL/6 mice with LPS induced inflammation through regulating PCSK9-LDLR pathway.
authors.affiliation: Colege of Veterinary Medicine, Hunan Agricultural University, Changsha, China. xhbzhb@yahoo.com
authors.forename: Hong-Bo
authors.initials: HB
authors.lastname: Xiao
authors.forename: Zhi-Liang
authors.initials: ZL
authors.lastname: Sun
authors.forename: Heng-Bo
authors.initials: HB
authors.lastname: Zhang
authors.forename: Da-Sheng
authors.initials: DS
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001599:Berberine / Q000494:pharmacology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism; D050171:Dyslipidemias / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D005260:Female; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D053582:Interleukin-1alpha / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008070:Lipopolysaccharides; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D010936:Plant Extracts / Q000494:pharmacology; D000071449:Proprotein Convertase 9; D043484:Proprotein Convertases / Q000378:metabolism; D011973:Receptors, LDL / Q000378:metabolism; D012697:Serine Endopeptidases / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053582:Interleukin-1alpha; D008055:Lipids; D008070:Lipopolysaccharides; D010936:Plant Extracts; D011973:Receptors, LDL; D014409:Tumor Necrosis Factor-alpha; D001599:Berberine; C075750:8-epi-prostaglandin F2alpha; D007371:Interferon-gamma; D015237:Dinoprost; C472126:Pcsk9 protein, mouse; D000071449:Proprotein Convertase 9; D043484:Proprotein Convertases; D012697:Serine Endopeptidases