Ethanolic extract of propolis inhibits atherosclerosis in ApoE-knockout mice.
BACKGROUND
The present study was undertaken to investigate the effects and underlying mechanism of ethanolic extract of propolis (EEP) on the development of atherosclerotic lesions in ApoE-/- mice.


METHODS
Eight-week-old male ApoE-/- mice fed a high-fat diet were treated with EEP (160 mg/kg/d) or vehicle (the same dose) respectively for 14 weeks. The serum levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were determined by enzymatic methods. Non-HDL-C was calculated as TC minus HDL-C. Serum interleukin-6 (IL-6), interleukin-17 (IL-17), endothelin (ET), inducible nitric oxide synthase (iNOS) and vascular endothelial growth factor (VEGF) were determined with enzyme-linked immunosorbent assay methods. Nitric oxide (NO) content was measured with an enzymatic nitrate reductase assay. Analyses of atherosclerotic lesions in whole aorta and aortic root sections were performed with plaque staining using Oil Red O.


RESULTS
Compared with the vehicle-treated group, serum contents of total cholesterol (TC), triglycerides (TG) and non-HDL-C reduced significantly by 31.88%, 21.01%, and 27.11% respectively in the EEP-treated group. Administration of EEP decreased the level of IL-6 and increased the level of IL-17 in ApoE-/- mice with a high-fat diet. Compared with the vehicle-treated group,EEP significantly reduced the levels of ET and VEGF,and showed a trend to increase NO and inhibit iNOS. In the ApoE-/- mice fed a high-fat diet, EEP significantly reduced atherosclerotic lesion development in the aortic root and whole aorta.


CONCLUSIONS
EEP can inhibit atherosclerotic lesion formation in ApoE-/- mice fed a high-fat diet possibly through modulating cholesterol, regulating inflammatory reaction,inhibiting ET and VEGF, and protecting vascular endothelial cells.
Yongqi
Y
Fang
Hui
H
Sang
Na
N
Yuan
Hongli
H
Sun
Shutong
S
Yao
Jiafu
J
Wang
Shucun
S
Qin
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics* / Q000378:metabolism; D050197:Atherosclerosis / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D000431:Ethanol / Q000737:chemistry; D020381:Interleukin-17 / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D018345:Mice, Knockout; D009569:Nitric Oxide / Q000097:blood; D052247:Nitric Oxide Synthase Type II / Q000097:blood; D058226:Plaque, Atherosclerotic / Q000188:drug therapy / Q000378:metabolism; D011429:Propolis / Q000494:pharmacology*; D014280:Triglycerides / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
D001057:Apolipoproteins E; D020381:Interleukin-17; D008075:Lipoproteins, HDL; D014280:Triglycerides; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D009569:Nitric Oxide; D000431:Ethanol; D011429:Propolis; D002784:Cholesterol; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse