| Aim To analyze the effect induced by hyperlipidemia, hyperhomocysteinemia andballoon injury alone or together on atherosclerosis forming process. To compare the efffectand difference of traditional drug--folicin intervening hyperlipidemia, hyperhomocysteinemiaand atherosclerosis with that of taurine through the observation of atherosclerosispathophysiological events, anatomic pathological and histological form, nanometer structurechange and expression of related factors. Further enrich and perfect the relevant basic theory,and providing new basis for atherosclerosis prevention and treatment.Methods1.56rabbits were divide into seven groups at random:normal control group(n=8) with ordinary rabbit granular feed. Injury control group (n=8)with ordinary rabbitgranular feed. Methionine group (n=8) with2%methionine granular feed. High fat group (n=8) with high fat granular feed. Model group (n=8) with high fat+2%methionine granularfeed. Folicin group (n=8)with high fat+2%methionine granular feed, and at the same timegive folicin tablet5mg/d. Taurine group (n=8) with high fat+2%methionine+1%taurinegranular feed. Experiment cycle last for12weeks for each group above. Except for the normalcontrol group, abdominal aortas of other groups were injured by balloon after2weeks.2.Blood was drawn for Tc,TG, LDL-c, HDL-c, Hcy, Ox-LDL, MMP-9test in0,2,12weeks.3. The rabbits were put to death after12weeks, abdominal aortas were detached out.Fresh artery tissue samples was intercepted as frozen section sample, transmission electronmicroscopy samples and tissue homogenate sample for oil red O dyeing, ultrathin slice preparation, half quantitative detection of MMP-9, NFKB.Part of tissue samples wereintercepted and fixed with10%-neutral formalin for24hours, dehydrated, transparentized,paraffined and embedded,sliced for H.E. stain, alkaline magenta dyeing, VCAM-1, NFKBimmunohistochemical stains; Surplus tissue was used for holistic oil red O dyeing4.Images were analyzed with Image-pro plus professional analysis software.Results1.blood lipid and homocysteine level: rabbit serum TG, Tc, HDL-c, LDL-c inhyperlipemia group, model group, folicin group, taurine group increased significantly (P <0.05)2weeks later compared with normal control group,and there was no significantdifference (P>0.05)with the level of12weeks later in each groups. HCY level in modelgroup and taurine group rised significantly compared with the normal control group (P <0.05)two weeks later, Hcy level in folicin group is lower, and there was significant differencecompared with model group (P <0.05), there wre no obvious change between Hcy level ineach group12weeks later with2weeks later (P>0.05).2. Abdominal aorta atheromatous plaque formation conditions in each group of rabbit:there was no significantly reduction in folicin group rabbit compared with model group (P>0.05) in abdominal aorta atheromatous plaques area; there was significantly reduction intaurine group rabbit compared with model group ((P <0.05).3. abdominal aorta pathological change in each group of rabbits: there were nosignificantly reduction (P>0.05)between folicin group rabbit with model group in abdominalaorta lining/intima-media thickness percentage. there were significantly reduction (P <0.05)between in taurine group rabbit with model group.4. The abdominal aorta lipid infiltration condition in rabbit: there was no significantmitigation (P>0.05)between folic acid group rabbit with model group in abdominal aorticlipid infiltration.Abdominal aortic lipid infiltration in taurine group significantly reducedcompared with model group (P <0.05).5The abdominal aorta elastic fiber change in rabbit: there were no significant difference between folic acid group with model group in abdominal aorta elastic fiber. Elastic fiberhyperplasia in taurine group rabbit obviously reduced compared with model group, and therewas no the elastic fiber and elastic plate degeneration,necrosis, fracture and dissolvephenomenon.6. The abdominal aorta change under electron microscopy in rabbit: mitochondria andendoplasmic reticulum remarkable hyperplasia, the mitochondrial membrane and creststructure damaged, swelling like empty bubbly, lysosome devoured fat, nucleus shrinked,chromatin gathered to edge. there was no significantly reduce in folicin group, lesions intaurine group significantly reduced.7.The rabbit serum atherosclerosis related factors measurements: compared with modelgroup, serum Ox-LDL in folic acid group did not significant decreased (P>0.05), but serumOx-LDL in taurine group rabbit lowered significantly (P <0.05). there are no significantdifference (P>0.05) between each group of rabbit in serum MMP-9,VCAM-1.8. Half quantitative detection of MMP-9, NFKB level in abdominal aorta tissuehomogenate: compared with model group, tissue homogenate MMP-9, NFKB in folicin grouprabbit did not significantly reduced (P>0.05), and tissue homogenate MMP-9, NFKB intaurine group rabbit reduced significantly (P <0.05). there was positive correlation betweenMMP-9with NFKB (r=0.89,P<0.05)in each group of rabbits.9.The abdominal aortic VCAM-1expression in rabbit: there was no significantdifference (P>0.05)between folic acid group with model group.VCAM-1positive cells intaurine group significantly lowered than that in model group (P <0.05).10. Abdominal aorta nuclear transcription factors KB expression in rabbit: there was nosignificant difference (P>0.05) between folic acid group rabbit with model group in NFKBpositive cells percentage. NFKB positive cells percentage in taurine group significantlyreduced compared with model group (P <0.05). Conclusion1.Hyperlipidemia can be formed with high fat granular feed in New Zealandbig-eared white rabbit in2weeks, hyperhomocysteinemia also can be formed with highmethionine granular feed in2weeks,and its height equivalent to the degree in12weeks.2.It can cause more fully atherosclerosis soft plaques model that three factors workingtogether for12weeks. This model can be used as atherosclerosis soft plaques model inducedby hyperlipemia and hyperhomocysteinemia that taurine and folicin intervene.3. Folicin can significantly reduce hyperhomocysteinemia, but can not improve thedegree, area of atherosclerosis soft plaques and expression of related factors.4.Taurine, as a kind of endogenous cells protective substances, although cannot reduceserum homocysteine levels, but improve the degree, area of atherosclerosis soft plaques andexpression of related factors. Probably it is related to such mechanism as resistance of lipidinfiltration, antioxidant stress, restrain vascular matrix remodeling, antagonist inflammation,suppressing injury reaction et al. |
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