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PANAX NOTOGINSENG SAPONINS ATTENUATE ATHEROSCLEROSIS IN RATS BY REGULATING THE BLOOD LIPID PROFILE AND AN ANTI‐INFLAMMATORY ACTION

1 Previous studies have reported on the anti‐atherosclerotic effects of Panax notoginseng saponins (PNS). The aim of the present study was to explore the molecular mechanisms responsible for the anti‐atherosclerotic effects of PNS and the inflammatory response. 2 Thirty rats were randomly divided into three groups, namely a control group, a group, in which zymosan A was used to induce inflammation (Zym group) and a PNS‐treated group. Rats in the three groups were administered liquid paraffin (i.p.), zymosan A (20 mg/kg, i.p., once every 3 days) or zymosan A and PNS (100 mg/kg, i.p., once daily), respectively. All animals were fed a high‐fat diet for 9 weeks. At scheduled times, rats were killed, blood was collected and the aorta was removed. Pathological changes in aortas were observed using Sudan IV staining and transmission electron microscopy. Serum lipids were measured enzymatically. Whole‐blood viscosity was observed at different shear rates. The expression of cardiovascular disease‐specific genes was determined using GEArray (SuperArray, Frederick, MA, USA). Western blotting was used to evaluate the expression levels of nuclear factor (NF)‐κB/p65 and its inhibitor IκBα in the aortic wall. 3 In the present study, typical pathological changes associated with atherosclerosis in rats following induction by zymosan A were alleviated by PNS treatment. In the PNS‐treated group, there was a marked reduction in total serum cholesterol, triglycerides and blood viscosity. In addition, PNS treatment significantly decreased the gene expression of some inflammatory factors, such as integrins, interleukin (IL)‐18, IL‐1β and matrix metalloproteinases 2 and 9. The expression of NF‐κB/p65 was attenuated, whereas the expression of IκBα was significantly increased, after treatment with PNS. 4 In conclusion, it appears that PNS exerts its therapeutic effects on atherosclerosis through an anti‐inflammatory action and regulation of the blood lipid profile and that an NF‐κB signalling pathway is involved.