Bee venom reduces atherosclerotic lesion formation via anti-inflammatory mechanism.
The components of bee venom (BV) utilized in the current study were carefully scrutinized with chromatography. Despite its well documented anti-inflammatory property, there are no reports regarding the influence of BV on the expression of cellular adhesion molecules in the vascular endothelium. A great amount of information exists concerning the effects of an atherogenic diet on atherosclerotic changes in the aorta, but little is known about the molecular mechanisms and the levels of gene regulation involved in the anti-inflammatory process induced by BV. The experimental atherosclerosis was induced in mice by a lipopolysaccharide (LPS) injection and an atherogenic diet. The animals were divided into three groups, the NC groups of animals that were fed with a normal diet, the LPS/fat group was fed with the atherogenic diet and received intraperitoneal injections of LPS, and the LPS/fat + BV group was given LPS, an atherogenic diet and intraperitoneal BV injections. At the end of each treatment period, the LPS/fat + BV group had decreased levels of total cholesterol (TC) and triglyceride (TG) in their serum, compared to the LPS/fat group. The LPS/fat group had significant expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the serum, compared with the NC group (p < 0.05). The amount of cytokines reduced consistently in the BV treatment groups compared with those in LPS/fat group. BV significantly reduced the amount of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), transforming growth factor-β1 (TGF-β1) and fibronectin in the aorta, compared with the LPS/fat group (p < 0.05). A similar pattern was also observed in the heart. In conclusion, BV has anti-atherogenic properties via its lipid-lowering and anti-inflammatory mechanisms.
Department of Pathology, Catholic University of Daegu, Korea.
Woo-Ram
WR
Lee
Soo-Jung
SJ
Kim
Ji-Hyun
JH
Park
Kyung-Hyun
KH
Kim
Young-Chae
YC
Chang
Yoon-Yup
YY
Park
Kwang-Gill
KG
Lee
Sang-Mi
SM
Han
Joo-Hong
JH
Yeo
Sok Cheon
SC
Pak
Kwan-Kyu
KK
Park
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D056705:Apitherapy; D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D001514:Bee Venoms / Q000494:pharmacology* / Q000627:therapeutic use; D016207:Cytokines / Q000097:blood; D004041:Dietary Fats / Q000009:adverse effects*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005353:Fibronectins / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D008055:Lipids / Q000097:blood*; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D053773:Transforming Growth Factor beta1 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D000893:Anti-Inflammatory Agents; D001514:Bee Venoms; D016207:Cytokines; D004041:Dietary Fats; D005353:Fibronectins; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D008055:Lipids; D008070:Lipopolysaccharides; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1