PMID- 21157115 OWN - NLM STAT- MEDLINE DCOM- 20111011 LR - 20190608 IS - 1880-3873 (Electronic) IS - 1340-3478 (Linking) VI - 18 IP - 4 DP - 2011 TI - Housefly maggots (Musca domestica) protein-enriched fraction/extracts (PE) inhibit lipopolysaccharide-induced atherosclerosis pro-inflammatory responses. PG - 282-90 AB - AIM: 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 (IFNgamma), tumor necrosis factor alpha (TNFalpha) and interleukin-1alpha (IL-1alpha)) 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 TNFalpha, IL-1alpha 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 TNFalpha, IL-1alpha and MCP-1 in LPS-induced macrophages was inhibited by different concentrations of PE (p< 0.01). CONCLUSION: 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. FAU - Chu, Fu-Jiang AU - Chu FJ AD - Guangdong Key Laboratory for Bioactive Drugs Research, Guangdong Pharmaceutical University, Guangzhou, China. FAU - Jin, Xiao-Bao AU - Jin XB FAU - Zhu, Jia-Yong AU - Zhu JY LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20101210 PL - Japan TA - J Atheroscler Thromb JT - Journal of atherosclerosis and thrombosis JID - 9506298 RN - 0 (Cytokines) RN - 0 (Insect Proteins) RN - 0 (Lipids) RN - 0 (Lipopolysaccharides) RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - Animals MH - Atherosclerosis/chemically induced/*drug therapy MH - Blood Vessels/pathology MH - Cells, Cultured MH - Cholesterol/administration & dosage MH - Cytokines/blood MH - Houseflies/*chemistry MH - Inflammation/*prevention & control MH - Insect Proteins/isolation & purification/pharmacology/*therapeutic use MH - Larva/*chemistry MH - Lipids/blood MH - Lipopolysaccharides MH - Macrophages/drug effects MH - Mice EDAT- 2010/12/16 06:00 MHDA- 2011/10/12 06:00 CRDT- 2010/12/16 06:00 PHST- 2010/12/16 06:00 [entrez] PHST- 2010/12/16 06:00 [pubmed] PHST- 2011/10/12 06:00 [medline] AID - JST.JSTAGE/jat/5991 [pii] AID - 10.5551/jat.5991 [doi] PST - ppublish SO - J Atheroscler Thromb. 2011;18(4):282-90. doi: 10.5551/jat.5991. Epub 2010 Dec 10.