Atherosclerosis lesion is accelerated by persistent systemic inflammation but attenuated by saponins from Panax Notoginseng in rabbits*

ObjectiveTo explore the roles of persistent systemic inflammation in atherosclerosis and the effects of saponins of Panax Notoginseng (PNS) on this process in rabbits.MethodsThirty rabbits were divided randomly and equally into 6 groups, i.e., control, high-fat diet, inflammation, aspirin, PNS and simple-inflammation group. All the animals except that in control group and simple-inflammation group were fed with high-fat diet for 8 weeks. Based on that, rabbits in inflammation, aspirin and PNS groups were treated with zymosan injection (10 mg/kg, i.p.). Normal saline was given to rabbits in control group. Besides zymosan injection, animals in aspirin and PNS group were administrated with aspirin (12 mg/kg, i.g.) and PNS (120 mg/kg, i.g.) respectively. The animals in simple-inflammation group were treated with zymosan injection (10mg/kg, i.p.) and fed with normal diet. The atherosclerosis lesion in aortas was observed by Sudan IV staining. Serum total cholesterol, triglyceride (TG), TNF-α and activity of post-heparin lipoprotein lipase (LPL) were measured at the end of the 4th and 8th week after an overnight fast.ResultsCompared with high-fat diet group, the area of atherosclerosis lesion, serum TG and TNF-αwere markedly increased in rabbits of inflammation group, and the activity of LPL was decreased remarkably. Serum TNF-α level was negatively correlated with the activity of post-heparin LPL (r = –0.708, P < 0.01). The area of atherosclerosis, serum TG and TNF-αwere decreased in aspirin and PNS group compared with that in inflammation group, and the activity of LPL was increased remarkably. Compared with control group, serum TG and TNF-α were markedly increased in simple-inflammation group, while LPL activity was decreased. Atherosclerotic lesion did not occur in simple-inflammation group.ConclusionsPersistent systemic inflammation could accelerate the formation of atherosclerosis lesion in aortas, which partly depend on the decreasing of the activity of post-heparin lipoprotein lipase. PNS could improve the changes caused by inflammation.