title: Housefly maggots (Musca domestica) protein-enriched fraction/extracts (PE) inhibit lipopolysaccharide-induced atherosclerosis pro-inflammatory responses.
abstract: OBJECTIVE
  To investigate the effects of housefly maggot (Musca domestica) protein-enriched fraction/extracts (PE) on lipopolysaccharide (LPS)-induced atherosclerosis (AS) pro-inflammatory responses in mice and macrophages.
  
  
  METHODS
  The mouse model of AS was established by feeding a cholesterol-enriched diet and inducing by LPS. Changes in the levels of blood lipids (total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL)) and pro-inflammatory cytokines (interferon-gamma (IFNγ), tumor necrosis factor alpha (TNFα) and interleukin-1alpha (IL-1α)) were determined. Histomorphometric analysis of the pathological condition of the artery was also carried out. The macrophages were stimulated by LPS in the presence or absence of PE, and then the levels of TNFα, IL-1α and monocyte chemotactic protein 1 (MCP-1) in cell culture supernatant were measured.
  
  
  RESULTS
  Compared with the negative control group, the levels of three pro-inflammatory cytokines were significantly enhanced in the PE treatment group (p< 0.01). The concentrations of TC, TG and LDL were lower in the PE treatment group than in the negative control group (p< 0.01). HDL concentration in the PE treatment group was higher than in the negative control group (p< 0.01). Histomorphometric analysis showed that the thickness of the intima and media area, as well as the area ratio of the intima to media in the PE treatment group were lower than in the negative control group (p< 0.01). The expression of TNFα, IL-1α and MCP-1 in LPS-induced macrophages was inhibited by different concentrations of PE (p< 0.01).
  
  
  CONCLUSIONS
  These results indicate that PE potently inhibited multiple pro-inflammatory responses in experimental atherosclerosis lesions in vivo, and possessed anti-pro-inflammatory properties in vitro.
authors.affiliation: Guangdong Key Laboratory for Bioactive Drugs Research, Guangdong Pharmaceutical University, Guangzhou, China.
authors.forename: Fu-Jiang
authors.initials: FJ
authors.lastname: Chu
authors.forename: Xiao-Bao
authors.initials: XB
authors.lastname: Jin
authors.forename: Jia-Yong
authors.initials: JY
authors.lastname: Zhu
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000139:chemically induced / Q000188:drug therapy*; D001808:Blood Vessels / Q000473:pathology; D002478:Cells, Cultured; D002784:Cholesterol / Q000008:administration & dosage; D016207:Cytokines / Q000097:blood; D006793:Houseflies / Q000737:chemistry*; D007249:Inflammation / Q000517:prevention & control*; D019476:Insect Proteins / Q000302:isolation & purification / Q000494:pharmacology / Q000627:therapeutic use*; D007814:Larva / Q000737:chemistry*; D008055:Lipids / Q000097:blood; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects; D051379:Mice
chemical_list: D016207:Cytokines; D019476:Insect Proteins; D008055:Lipids; D008070:Lipopolysaccharides; D002784:Cholesterol