Anti-atherosclerosis Effects Of Momordicin Relating Down Regulating Inflammatory Factor

OBJECTIVE To explore the anti-atherosclerosis effects of momordicin on ApoE-/-Mice and further analysis the molecular mechanism related to inflammatory factor.METHODS40male apoE-/-mice,6weeks old,18.1±1.4g, was randomly dividedinto four groups(10animals of each group):①normal food group[normal food+PBS0.1ml/2d, intraperitoneal injection (IP)];②high fat high cholesterol group (high fathigh cholesterol food+PBS0.1ml/2d, IP);③high fat high cholesterol andMomordicin group (high fat high cholesterol+Momordicin0.1ml/2d, IP);④normalfood and Momordicin group (normal food+Momordicin0.1ml/2d, IP). Animals fromhigh fat high cholesterol group and high fat high cholesterol and Momordicin groupwere fed with western food which concluding10%fat and2%cholesterol. Afterfeeding12weeks, all mice were anesthetized by0.2～0.3ml Urethane (20%) andremoved eyeball in order to obtain blood preparation. The Hematoxylin/Eosin dyeingof paraffin section was used to detect the area of atherosclerotic plaque of apoE-/-mice aortic root transaction. Gene and protein expression was analyzed bysemi-quantitative RT-PCR and Western blot, respectively. Level of inflammatoryfactor (IL-1β,TNF-α, IL-6,INF-γ) and anti-inflammatory factor(IL-10) weremeasured by ELISA, IkB expression of aorta was analyzed by immunohistochemistry.RESULTS Compared with high fat high cholesterol group, the aorta atheroscleroticlesion area of momordicin treat group is smaller obviuously(p<0.01,n=5),interestingly,the aorta atherosclerotic lesion area of normal food and momordicin group is smallernotablely than normal food group(p<0.05,n=5). After fed with high fat highcholesterol for about12weeks, inflammatory factor (IL-1β,TNF-α, IL-6,INF-γ)levelincreased, and this tendency can be inhibited by momordicin intervention, inflammatory factor and anti-inflammatory factor were regulated to their equilibriumpoint(inflammatory factor≈41, IL-10=32), but the level of IL-10can not beup-regulated. The expression of TNF-α and IL-1β of momordicin treat group werelower obviously than high fat high cholesterol group both mRNA and protein level inartery wall. Compared with high fat high cholesterol group, no effect was found onNF-kB mRNA expression in momordicin treat group, but nuclear translocation ofNF-kB was inhibited by momordicin treated. After fed with high fat high cholesterolfor about12weeks, Ik-B in artery wall was reduced remarkably compared withnormal food group(0.19±0.05vs0.74±0.15，P<0.05，n=3), but this reduction can beinhibited obviously by momordicin intervention(0.19±0.05vs0.36±0.07，P<0.01，n=3).CONCLUSIONS Atherosclerotic lesions in apoE-/-mice were attenuated byadministration of momordicin; It maybe related to down-regulating inflammatoryfactor level both in serum and artery wall, and inhibit nuclear translocation of NF-kBand degradation of IkB.