Expression of group Ⅱ a secretory phospholipase A2 in atherosclerotic rat model

SUN Chang-qing; LI Wei-hua; CHEN Qing-fu; GUO Li-rong

doi:10.3760/cma.j.issn.1673-4777.2013.02.003

Abstract：Objective To detect the expression of group Ⅱ a secretory phospholipase A2 (sPLA2 Ⅱ a) inthe aorta of atherosclerosis (AS) rat model and to investigate its relation to tumor necrosis factor α (TNF-α) andinterleukin 6 (IL-6).To study the influence of simvastatin on sPLA2 Ⅱ a.Methods The athemsclerosis model inrats was set up by feeding with high cholesterol diet for six week.Meanwhile animals were randomized to receiveeither no treatment or simvastatin [5 mg/(kg · d)].The expression of sPLA2 Ⅱ a was studied by immunohisto-chemistry.The levels of TNF-α and IL-6 in serum were measured by enzyme linked immunosorbent assay.ResultsThe total cholesterol (TC),triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) level of high fatdiet group [(TG:(1.9 ± 0.5) mmol/L,TC:(5.82 ± 1.13) mmol/L,LDL-C:(3.97 ± 0.78) mmol/L] wassignificantly higher than those in control group[TG:(1.5 ± 0.6)mmol/L,TC:(1.98 ± 0.26) mmol/L,LDL-C:(0.50 ± 0.16) mmol/L,P ＜ 0.01],simvastatin decrease the level of TC,TG and LDL-C [TC:(3.78 ±0.59) mmol/L,TG:(0.8 ± 0.4) mmol/L,LDL-C:(1.49 ± 0.62) mmol/L,P ＜ 0.05].It showed that the levelsof TNF-α and IL-6 in serum in high fat diet group[TNF-α:(15.48 ± 1.03) ng/L,IL-6:(72.0 ±7.5)ng/L] weresignificantly higher than those in control group [TNF-α:(8.40 ± 0.28) ng/L,IL-6:(25.1 ± 2.3)ng/L,P ＜0.01]; simvastatin decreased the levels of TNF-α and IL-6 [TNF-α:(10.54 ± 1.96)ng/L,IL-6:(40.2 ±20.2) ng/L,P ＜0.01].sPLA2 Ⅱ a was present in smooth muscle cell and plaque of aorta.In contrast,sPLA2 Ⅱ aexpression in aorta was much higher in high fat diet group than those in control group,expression of the enzyme inaorta was decreased in simvastatin group compared to high fat diet group.Conclusions This result supports thehypothesis that sPLA2 Ⅱ a may play a significant role in the pathogenesis of AS.Simvastatin could relieve theprocess of AS by decreasing the expression level of sPLA2 Ⅱ a.