The effects of oleanolic acid on atherosclerosis in different animal models

• Published in: Acta biochimica et biophysica Sinica 2017-04, Vol.49 (4), p.349-354
• Main Authors: Luo, Hanqiong, Liu, Jine, Ouyang, Qiong, Xuan, Chunxiao, Wang, Lanlan, Li, Tingting, Liu, Jun
• Format: Article
• Language: English
• Subjects: Animals; Atherosclerosis - blood; Atherosclerosis - genetics; Atherosclerosis - prevention & control; Cholesterol - blood; Cholesterol, HDL - blood; Cholesterol, LDL - blood; Disease Models, Animal; Gene Expression - drug effects; Lipid Metabolism - genetics; Mice, Inbred C57BL; Mice, Knockout; Molecular Structure; Oleanolic Acid - chemistry; Oleanolic Acid - pharmacology; PPAR gamma - genetics; Rabbits; Receptors, Adiponectin - genetics; Receptors, LDL - deficiency; Receptors, LDL - genetics; Reverse Transcriptase Polymerase Chain Reaction; Species Specificity
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmx013

In the present study, three animal models, including C57BL/6J mice, low-density lipoprotein recep- tor knockout （LDLR-/-） mice, and rabbit that mimicked atherosclerosis, were established to investi- gate the inhibitory effect of oleanotic acid （OA） on atherosclerosis. In rabbit model, serum total cholesterol （TC）, triglyceride, low density lipoprotein cholesterol （LDL-C）, and high density lipoprotein cholesterol （HDL-C） were measured. Carotid artery lesions were isolated for histological analysis. The red oil O and hematoxylin-eosin staining in liver were examined. The messenger ribonucleicacid （mRNA） levels of PPARy, AdipoR1, and AdipoR2 related to lipid metabolism were determined. Compared with model group, OA and atorvastatin significantly lowered the levels of TC and LDL-C. The result of red oil O staining showed that OA and atorvastatin had similar effect on reducing the accumulation of lipid. Histological result demonstrated that OA reduced the thickness of intima. AdipoRl was markedly increased, while AdipoR2 was remarkably decreased in OA group com- pared with that in the control group of the rabbit model. In LDLR-/- mouse model, lipid parameters in blood and mRNA levels of PPART, AdipoRl, and AdipoR2 were measured. It was found that OA exhibited similar effects as atorvastatin including reduced TG, LDL-C, and enhanced HDL-C. Notably, OA elevated the levels of AdipoR1 and PPART. At the same time, OA decreased TC and LDL-C in C57BL/6J mice model. Our results in three different animal models all revealed that OA retarded the development of atherosclerosis by influencing serum lipid levels, lipid accumulation in liver and intimal thickening of artery. And the underlying mechanism of OA on atherosclerosis may involve in lipid metabolism genes： PPARy, AdipoRl, and AdipoR2.